Immunology Graduate Program

Meet the Faculty

A photo of Theresa Alenghat.

Theresa Alenghat, VMD, PhD

Theresa Alenghat, VMD, PhD, investigates central epigenomic pathways that regulate epithelial and immune cell homeostasis in the context of intestinal health and disease. The goal of her research is to provide insight into mechanisms underlying the host-commensal relationship and how this level of regulation affects the development of chronic diseases such as inflammatory bowel disease.
Visit the Alenghat Lab.

513-803-7498 theresa.alenghat@cchmc.org

A photo of Theresa Alenghat.

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Theresa Alenghat, VMD, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-803-7498

Email theresa.alenghat@cchmc.org

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Research Interests

Visit the Alenghat Lab.

Education and Training

BS: Brown University, Providence, RI, 1999.

VMD: University of Pennsylvania, Philadelphia, PA, 2003.

PhD: University of Pennsylvania, Philadelphia, PA, 2007.

Residency: Anatomic Pathology, University of Pennsylvania, Philadelphia, PA.

Certification: Diplomate ACVP, 2011.

View PubMed Publications

Kelly D, Kotliar M, Woo V, Jagannathan S, Whit J, Moncivaiz J, Aronow BJ, Dubinsky MC, Hyams JS, Markowitz JF, Baldassano RN, Stephens MC, Walters TD, Kugathasan S, Haberman Y, Sundaram N, Rosen MJ, Helmrath M, Karns R, Barski A, Denson LA, Alenghat T. Microbiota-sensitive epigenetic signature predicts inflammation in Crohn’s disease. JCI Insight. 2018.

Whitt J, Woo V, Lee P, Moncivaiz J, Haberman Y, Denson LA, Tso P, Alenghat T. Disruption of epithelial HDAC3 in intestine prevents diet-induced obesity in mice. Gastroenterology. 2018.

Jiang TT, Shao T, Gladys Ang WX, Kinder JM, Turner L, Pham G, Whitt J, Alenghat T, Way SS. Commensal fungi replace the protective benefits of intestinal bacteria. Cell Host and Microbe. 2017;22:809-816.

Navabi N, Whitt J, Wu S, Woo V, Moncivaiz J, Jordan MB, Vallance BA, Way SS, Alenghat T. Epithelial histone deacetylase 3 instructs intestinal immunity by coordinating local lymphocyte activation. Cell Reports. 2017;19:1165-1175.

Woo V, Alenghat T. Host-microbiota interactions: Epigenomic regulation. Current Opinion in Immunology. 2017;44:52-60.

Gray J, Oehrle K, Worthen G, Alenghat T, Whitsett J, Deshmukh H. Intestinal commensal bacteria direct the development of lung mucosal immunity and promote newborn’s resistance to infections. Sci Transl Med. 2017;9(376),eaaf9412.

Whitsett J, Alenghat T. Respiratory epithelial cells orchestrate pulmonary innate immunity. Nature Immunology. 2015;16:27-35.

Alenghat T, Osborne LC, Saenz SA, Kobuley D, Ziegler CG, Mullican SE, Choi I, Grunberg S, Sinha R, Wynosky-Dolfi M, Snyder A, Giacomin PG, Joyce KL, Hoang TB, Bewtra M, Brodsky IE, Sonnenberg GF, Bushman FD, Won K, Lazar MA, Artis D. Histone Deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis. Nature. 2013 Dec 5;504(7478):153-7.

Sonnenberg GF, Monticelli LA, Alenghat T, Fung TC, Hutnick NA, Kunisawa J, Shibata N, Grunberg S, Sinha R, Zahm AM, Tardif MR, Sathaliyawala T, Kubota M, Farber DL, Collman RG, Shaked A, Fouser LA, Weiner DB, Tessier PA, Friedman JR, Kiyono H, Bushman FD, Chang K, Artis D. Innate lymphoid cells orchestrate anatomical containment of lymphoid-resident commensal bacteria and prevent systemic immune activation. Science. 2012 Jun 8;336(6086): 1321-5.

Alenghat T, Meyers K, Mullican SE, Leitner K, Adeniji-Adele A, Avila J, Bućan M, Ahima RS, Kaestner KH, Lazar MA. Nuclear receptor corepressor and histone deacetylase 3 govern circadian metabolic physiology. Nature. 2008 Dec 18;456(7224): 997-1000.

A photo of Artem Barski.

Artem Barski, PhD Director, Epigenomics Data Analysis Core

Artem Barski, PhD, uses cutting-edge genomic technologies (such as ChIP-Seq and RNA-Seq) to understand contribution of epigenetic mechanisms and polymerase stalling to T cell activation, differentiation and to formation of T cell memory.
Visit the Barski Lab.

513-636-1851 artem.barski@cchmc.org

A photo of Artem Barski.

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Artem Barski, PhD

Director, Epigenomics Data Analysis Core

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-636-1851

Email artem.barski@cchmc.org

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Research Interests

Epigenetics; epigenomics; immunology; T cell memory

Visit the Barski Lab.

Artem Barski, PhD, is interested in epigenomics and transcriptional regulation of gene expression. His PhD at the University of Southern California was focused on transcriptional regulation in osteoblasts. During his post-doctoral training in Keji Zhao lab at NIH, Dr. Barski took part in the development of ChIP-Seq, a revolutionary method that combines ChIP with the next-generation sequencing. ChIP-Seq allows genome-wide mapping of chromatin modifications and transcription factor binding sites with resolution and sensitivity far exceeding older methods. Since his arrival to Cincinnati Children’s Hospital Medical Center in 2011, Dr. Barski is working on epigenomics of immunological memory. His laboratory is also developing both wet lab and computational approaches to the study of epigenomics and runs Cincinnati Children's Epigenomics Data Analysis Core.

Dr. Barski has publications in prestigious journals including Cell, Nature Structural and Molecular Biology Genome Biology and others. He is a recipient of NHLBI Career Transition Award (K22) and NIH Director’s New Innovator Award (DP2).

Education and Training

BS/MS: Moscow State University, Department of Chemistry, Moscow, Russia, 2000.

PhD: University of Southern California, Los Angeles, CA, 2006.

Fellowship: National Institutes of Health (NIH), National Heart Lung, and Blood Institute (NHLBI), Bethesda, MD, 2011.

View PubMed Publications

Barski A, Cuddapah S, Kartashov AV, Liu C, Imamichi H, Yang W, Peng W, Lane HC, Zhao K. Rapid Recall Ability of Memory T cells is Encoded in their Epigenome. Sci Rep. 2017 Jan 5;7:39785.

Kartashov AV, Barski A. BioWardrobe: an integrated platform for analysis of epigenomics and transcriptomics data. Genome Biol. 2015 Dec 7;16(1):158.

Sin H-S, Kartashov AV, Hasegawa K, Barski A, Namekawa SH. Poised chromatin and bivalent domains facilitate the mitosis-to-meiosis transition in the male germline. BMC Biol. 2015;13:53.

Rochman Y, Yukawa M, Kartashov AV, Barski A. Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig. PLoS One. 2015;10(4):e0122198.

Hasegawa K, Sin H-S, Maezawa S, Broering TJ, Kartashov AV, Alavattam KG, Ichijima Y, Zhang F, Bacon WC, Greis KD, Andreassen PR, Barski A, Namekawa S. SCML2 Establishes the Male Germline Epigenome through Regulation of Histone H2A Ubiquitination. Dev Cell. 2015;(5):574–88.

Rochman Y, Yukawa M, Kartashov AV, Barski A. Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig. PLoS One. 2015;10(4):e0122198.

Barski A, Chepelev I, Liko D, Cuddapah S, Fleming AB, Birch J, Cui K, White RJ, Zhao K. Pol II and its associated epigenetic marks are present at Pol III-transcribed noncoding RNA genes. Nat Struct Mol Biol. 2010 May;17(5):629-34.

Barski A, Jothi R, Cuddapah S, Cui K, Roh TY, Schones DE, Zhao K. Chromatin poises miRNA- and protein-coding genes for expression. Genome Res. 2009 Oct;19(10):1742-51

Barski A, Zhao K. Genomic location analysis by ChIP-Seq. J Cell Biochem. 2009 May 1;107(1):11-8.

Barski A, Cuddapah S, Cui K, Roh TY, Schones DE, Wang Z, Wei G, Chepelev I, Zhao K. High-resolution profiling of histone methylations in the human genome. Cell. 2007 May 18;129(4):823-37.

Barski A, Cuddapah S, Cui K, Roh T-Y, Schones DE, Wang Z, et al. High-resolution profiling of histone methylations in the human genome. Cell. 2007 May 18;129(4):823–37.

Direct Epigenetic Reprogramming of T Cells. Principal Investigator. National Institute of General Medical Sciences/National Institutes of Health New Innovator Award. Sep 2015-Sep 2020.

Epigenetic Mechanisms of Humoral Immune Deficiency in Kabuki Syndrome. Co-principal Investigator. Center for Pediatric Genomics. Jan 2016-Dec 2017.

Epigenomics Data Analysis Core Translational T1 grant. Principal Investigator. Center for Clinical and Translational Science and Technology. Jul 2015–Jun 2017.

A photo of Jorge Bezerra.

Jorge A. Bezerra, MD Director, Division of Gastroenterology, Hepatology and Nutrition

Jorge A. Bezerra, MD, investigates the genetic, cellular and molecular basis of biliary atresia and other cholangiopathies in children. His studies use animal models of disease to identify causes of tissue injury and to develop new therapies to stop progression of liver disease.
Visit the Bezerra Lab.

513-636-3008 jorge.bezerra@cchmc.org

A photo of Jorge Bezerra.

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Jorge A. Bezerra, MD

Director, Division of Gastroenterology, Hepatology and Nutrition

Medical Director, Pediatric Liver Care Center

Recruitment Director, Child Health Research Career Development Award

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-3008

Fax 513-636-5581

Email jorge.bezerra@cchmc.org

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Research Interests

Visit the Bezerra Lab.

Jorge A. Bezerra, MD, joined the Cincinnati Children's Hospital Medical Center Division of Gastroenterology, Hepatology and Nutrition in 1990, when he began his fellowship training in pediatric gastroenterology and nutrition and graduated in 1993.

From 1992-1994, Dr. Bezerra was a research scholar in the Division of Basic Sciences. He was appointed to the division in 1994 as an assistant professor within the UC Department of Pediatrics.

Dr. Bezerra completed his residency in pediatrics at the University of Arizona in Tucson, Arizona.

Dr. Bezerra has an active research career with his primary interests in molecular control of liver regeneration, biliary atresia, and genetic basis of intrahepatic cholestasis.

In addition to his research work, Dr. Bezerra is an active clinician for the outpatient GI clinical service and the inpatient liver service.

Education and Training

MD: Federal University Rio Grande Norte, Natal, Brazil, 1984.

Residency: University of Arizona, Tuscon, AZ, 1989.

Fellowship: Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, OH, 1994.

Certification: Pediatrics, Pediatric Gastroenterology, Hepatology and Nutrition.

View PubMed Publications

Bezerra JA. Biliary atresia in Brazil: where we are and where we are going. J Pediatr (Rio J). 2010 Nov-Dec;86(6):445-7.

Moyer K, Kaimal V, Pacheco C, Mourya R, Xu H, Shivakumar P, Chakraborty R, Rao M, Magee JC, Bove K, Aronow BJ, Jegga AG, Bezerra JA. Staging of biliary atresia at diagnosis by molecular profiling of the liver. Genome Med. 2010 May 13;2(5):33.

Kumar Mohanty S, Ivantes CA, Mourya R, Pacheco C, Bezerra JA. Macrophages are targeted by rotavirus in experimental biliary atresia and induce neutrophil chemotaxis via Mip2/Cxcl2. Pediatr Res. 2010 Jan 6.

Shivakumar P, Sabla GE, Whitington P, Chougnet CA, Bezerra JA. Neonatal NK cells target the mouse duct epithelium via Nkg2d and drive tissue-specific injury in experimental biliary atresia. J Clin Invest. 2009 Aug;119(8):2281-90.

Shanmukhappa K, Matte U, Degen JL, Bezerra JA. Plasmin-mediated proteolysis is required for hepatocyte growth factor activation during liver repair. J Biol Chem. 2009 May 8;284(19):12917-23.

Erickson N, Mohanty SK, Shivakumar P, Sabla G, Chakraborty R, Bezerra JA. Temporal-spatial activation of apoptosis and epithelial injury in murine experimental biliary atresia. Hepatology. 2008 May;47(5):1567-77.

Shivakumar P, Sabla G, Mohanty S, McNeal M, Ward R, Stringer K, Caldwell C, Chougnet C, Bezerra JA. Effector role of neonatal hepatic CD8+ lymphocytes in epithelial injury and autoimmunity in experimental biliary atresia. Gastroenterology. 2007 Jul;133(1):268-77.

Liu C, Aronow BJ, Jegga AG, Wang N, Miethke A, Mourya R, Bezerra JA. Novel resequencing chip customized to diagnose mutations in patients with inherited syndromes of intrahepatic cholestasis. Gastroenterology. 2007 Jan;132(1):119-26.

Campbell KM, Arya G, Ryckman FC, Alonso M, Tiao G, Balistreri WF, Bezerra JA. High prevalence of alpha-1-antitrypsin heterozygosity in children with chronic liver disease. J Pediatr Gastroenterol Nutr. 2007 Jan;44(1):99-103.

Shanmukhappa K, Sabla GE, Degen JL, Bezerra JA. Urokinase-type plasminogen activator supports liver repair independent of its cellular receptor. BMC Gastroenterol. 2006 Nov 29;6:40.

Charles C. Caldwell, PhD

focuses his research around trauma, sepsis and inflammation.

513-558-1974 caldwecs@ucmail.uc.edu

A photo of Jose Cancelas Perez.

Jose A. Cancelas Perez, MD, PhD Director, Hoxworth Blood Center

Jose A. Cancelas Perez, MD, PhD, focuses on the study of blood-forming cells during the process of adult hematopoiesis. In particular, hematopoietic stem cells (HSC) attract clinical interest because of their potential use in stem cell and gene therapy, and because of their involvement in leukemia.
Visit the Cancelas Lab.

513-558-1324 jose.cancelas@uc.edu

A photo of Claire Chougnet.

Claire A. Chougnet, PhD

Claire A. Chougnet, PhD, aims to understand T cell function and dysfunction at a molecular level in human disease, with a focus on defining the molecular mechanisms that underlie T cell dysfunction in HIV/AIDS, defining the molecular mechanisms responsible for immune dysfunction in aging, and understanding the development of T cell responses in very early life.
Visit the Chougnet Lab.

513-636-8847 claire.chougnet@cchmc.org

A photo of Claire Chougnet.

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Claire A. Chougnet, PhD

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-8847

Fax 513-636-4278

Email claire.chougnet@cchmc.org

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Research Interests

Visit the Chougnet Lab.

Education and Training

DPharm: Université Paris XI, Paris, France, 1980.

CES (French specialized degrees; clinical biologist): Immunology, Hematology, Bacteriology-Virology, Parasitology, 1984.

PhD: Université Paris V, 1991.

View PubMed Publications

Lages CS, Lewkowich I, Sproles A, Wills-Karp M, Chougnet C. Partial restoration of T-cell function in aged mice by in vitro blockade of the PD-1/ PD-L1 pathway. Aging Cell. 2010 Oct;9(5):785-98. doi: 10.1111/j.1474-9726.2010.00611.x.

Miethke AG, Saxena V, Shivakumar P, Sabla GE, Simmons J, Chougnet CA. Post-natal paucity of regulatory T cells and control of NK cell activation in experimental biliary atresia. J Hepatol. 2010 May;52(5):718-26.

Presicce P, Moreno-Fernandez ME, Lages CS, Orsborn KI, Chougnet CA. Association of two clones allows for optimal detection of human FOXP3. Cytometry A. 2010 Jun;77(6):571-9.

Moreno-Fernandez ME, Zapata W, Blackard JT, Franchini G, Chougnet CA. Human regulatory T cells are targets for human immunodeficiency Virus (HIV) infection, and their susceptibility differs depending on the HIV type 1 strain. J Virol. 2009 Dec;83(24):12925-33.

Shivakumar P, Sabla GE, Whitington P, Chougnet CA, Bezerra JA. Neonatal NK cells target the duct epithelium via Nkg2d and drive the tissue-specific injury in biliary atresia. J Clin Invest. 2009 Aug;119(8)2281-90.

Nyakeriga AM, Fichtenbaum CJ, Goebel J, Nicolaou SA, Conforti L, Chougnet CA. Engagement of the CD4 receptor affects the redistribution of lck to the immunological synapse in primary T cells: implications for T cell activation during HIV-1 infection. J Virol. 2009 Feb;83(3):1193-200.

Boasso A, Shearer GM, Chougnet C. Immune dysregulation in HIV infection: know it, fix it, prevent it? J Intern Med. 2009, 265(1):78-96. Review.

Lages CS, Suffia I, Velilla P, Huang B, Warshaw G, Hildeman D, Belkaid Y, Chougnet C. Functional regulatory T cells accumulate in aged hosts and promote reactivation of chronic infectious disease reactivation. J Immunol. 2008;181(3):1835-48.

Velilla PA, Shata MT, Lages CS, Ying J, Fichtenbaum CJ, Chougnet C. Effect of intrauterine HIV-1 exposure on the frequency and phenotype of uninfected newborns’ dendritic cells. Clin Immunol. 2008;126:243-50.

Li S, Gowans EJ, Chougnet C, Plebanski M, Dittmer U. Natural regulatory T cells and persistent viral infection. J Virol. 2008;82:21-30. Review.

George Deepe, MD

focuses on the analysis of the protective immune response to the pathogenic fungus, Histoplasma capsulatum. His lab endeavors to determine the influence of cytokines and T cell subpopulations on host control of fungus. Using a mouse model to examine lungs which are the portal of entry for this fungus, our current studies investigate the role of chemokines and their receptors in host control of this fungus.
Visit the Deepe Lab.

513-558-4704 george.deepe@uc.edu

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George Deepe, MD

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-558-4704

Email george.deepe@uc.edu

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Host response to fungi

Education and Training

AB: Kenyon College, English and Biology, 1971.

MD: University of Cincinnati College of Medicine, 1976.

View PubMed Publications

Kroetz DN, Deepe GS Jr. An aberrant thymus in CCR5-/- mice is coupled with an enhanced adaptive immune response in fungal infection. J Immunol. 2011 May 15;186(10):5949-55.

Szymczak WA, Deepe GS Jr. Antigen-presenting dendritic cells rescue CD4-depleted CCR2-/- mice from lethal Histoplasma capsulatum infection. Infect Immun. 2010 May;78(5):2125-37.

Kroetz DN, Deepe GS Jr. CCR5 dictates the equilibrium of proinflammatory IL-17+ and regulatory Foxp3+ T cells in fungal infection. J Immunol. 2010 May 1;184(9):5224-31.

Szymczak WA, Deepe GS Jr. The CCL7-CCL2-CCR2 axis regulates IL-4 production in lungs and fungal immunity. J Immunol. 2009 Aug 1;183(3):1964-74.

McCormack FX, Gibbons R, Ward SR, Kuzmenko A, Wu H, Deepe GS Jr. Macrophage-independent fungicidal action of the pulmonary collectins. J Biol Chem. 2003 Sep 19;278(38):36250-6.

Gomez FJ, Woodward EO, Pilcher-Roberts R, Gibbons RS, Deepe GS Jr. V beta 6+ and V beta 4+ T cells exert cooperative activity in clearance of secondary infection with Histoplasma capsulatum. J Immunol. 2001 Feb 15;166(4):2855-62.

Allendoerfer R, Deepe GS Jr. Regulation of infection with Histoplasma capsulatum by TNFR1 and -2. J Immunol. 2000 Sep 1;165(5):2657-64.

Deepe GS Jr, Gibbons R, Woodward E. Neutralization of endogenous granulocyte-macrophage colony-stimulating factor subverts the protective immune response to Histoplasma capsulatum. J Immunol. 1999 Nov 1;163(9):4985-93.

Allendörfer R, Brunner GD, Deepe GS Jr. Complex requirements for nascent and memory immunity in pulmonary histoplasmosis. J Immunol. 1999 Jun 15;162(12):7389-96.

Gomez FJ, Cain, JA, Gibbons R, Allendoerfer R, and Deepe GS, Jr. Vβ4+T cells exert protection in murine in pulmonary histoplasmosis. J Clin Invest. 1998;102:984-995.

A photo of Senad Divanovic.

Senad Divanovic, PhD

Senad Divanovic, PhD, investigates the molecular mechanisms underlying the regulation of innate immune signaling and inflammation in: (a) development and progression of obesity; (b) development and progression of non-alcoholic fatty liver disease; and (b) induction of preterm birth. These studies, range from reductive analysis of TLR ligand signaling and challenge to the role of IL-17 axis to diverse experimental models of obesity and infection.
Visit the Divanovic Lab.

513-636-0286 senad.divanovic@cchmc.org

A photo of Senad Divanovic.

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Senad Divanovic, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-0286

Email senad.divanovic@cchmc.org

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Clinical Interests

Innate immune responses; obesity; NAFLD; preterm birth; echocardiography; fetal cardiology; Cardiology Consult Service; General Cardiology Outpatient Clinic

Visit the Divanovic Lab.

Education and Training

BA: DePauw University, Greencastle, IN, 1998.

MS: Oklahoma State University, Stillwater, OK, 2000.

PhD: University of Cincinnati, Cincinnati, OH, 2005.

Post Doc: Cincinnati Children’s Hospital Medical Center, 2010

View PubMed Publications

Allen JL, Flick LM, Divanovic S, Jackson SW, Bram R, Rawlings D, Finkelman FD, Karp CL. Cutting Edge: Regulation of TLR4-driven B cell proliferation by RP105 is not B cell-autonomous. J Immunol. 2012;188:2065.

Korfhagen TR, Kitzmiller J, Chen G, Sridharan A, Haitchi HM, Hegde RS, Divanovic S, Karp CL, Whitsett JA. SAM-pointed domain ETS factor mediates epithelial cell-intrinsic innate immune signaling during airway mucous metaplasia. PNAS. 2012;109:16630.

Divanovic S, Sawtell NM, Trompette A, Warning JI, Dias A, Cooper AM, Yap GS, Arditi M, Shimada K, DuHadaway JB, Prendergast GC, Basaraba RJ, Mellor AL, Munn DH, Aliberti J, Karp CL. Opposing biological functions of tryptophan catabolizing enzymes during intracellular infection. J Infect Dis. 2012;205:152-61.

Divanovic S, Trompette A, Jamie I. Ashworth, Marepalli B. Rao, Karp CL. Therapeutic enhancement of protective immunity during experimental Leishmania major infection. PLoS Neglected Tropical Dis. 2011;5:e1316.

Sheridan R, Lampe K, Shanmukhappa SK, Putnam P, Keddache M, Divanovic S, Bezerra J, Hoebe K. Lampe1: an ENU-germline mutation causing spontaneous hepatosteatosis identified through targeted exon-enrichment and next-generation sequencing. PLoS One. 2011;6:e21979.

Trompette A, Divanovic S, Visintin A, Blanchard C, Hegde RS, Madan R, Torne PS, Wills-Karp M, Gioannini TL, Weiss JP, Karp CL. Allergenicity resulting from functional mimicry of a Toll-like receptor complex protein. Nature. 2009;457:585-8.

Divanovic S, Trompette A, Petiniot LK, Allen JL, Flick LM, Belkaid Y, Madan R, Haky JJ, Karp CL. Regulation of TLR4 signaling and the host interface with pathogens and danger: the role of RP105. J Leukocyte Biol. 2007;82:265-271.

Divanovic S, Trompette A, Atabani SF, Madan R, Golenbock DT, Visintin A, Finberg RW, Tarakhovsky A, Vogel SN, Belkaid Y, Kurt-Jones EA, Karp CL. Inhibition of TLR4/MD-2 signaling by RP105/MD-1. J Endotoxin Res. 2005;11:363-8.

Divanovic S, Trompette A, Atabani SF, Madan R, Golenbock DT, Visintin A, Finberg RW, Tarakhovsky A, Vogel SN, Belkaid Y, Kurt-Jones EA, Karp CL. Negative regulation of Toll-like receptor 4 signaling by the Toll-like receptor homolog RP105. Nature Immunol. 2005;6:571-8.

Divanovic S, Lai ACK. Cytokine induction in human cord blood lymphocytes after pulsing with UV-inactivated influenza viruses. Immunology Lett. 2004;94:201-7.

A photo of Marie-Dominique Filippi.

Marie-Dominique Filippi, PhD Member, Division of Experimental Hematology & Cancer Biology

Marie-Dominique Filippi, PhD, is interested in dissecting the molecular mechanism of hematopoietic cell migration. Because hematopoietic cells are utilized for the therapy of multiple blood diseases and neutrophils are responsible for maintaining an immunocompetence status, understanding the molecular mechanism of normal hematopoietic cell functions is of potential therapeutic importance.
Visit the Filippi Lab.

513-636-0991 Marie-Dominique.Filippi@cchmc.org

A photo of Lee Grimes.

H. Leighton (Lee) Grimes, PhD Director, Cancer Pathology Program, Division of Experimental Hematology & Division of Pathology

H. Leighton (Lee) Grimes, PhD, focuses on the transcriptional control of normal and malignant hematopoiesis. The goal of his research is to understand how normal blood cells are formed, and to use this information to dissect the molecular pathogenesis of marrow failure and leukemia.
Visit the Grimes Lab.

513-636-6089 lee.grimes@cchmc.org

A photo of Lee Grimes.

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H. Leighton (Lee) Grimes, PhD

Director, Cancer Pathology Program, Division of Experimental Hematology & Division of Pathology

Co-Leader, Program in Hematologic Malignancies of Cincinnati Children's Hospital Medical Center, Cancer and Blood Diseases Institute

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-6089

Fax 513-636-5355

Email lee.grimes@cchmc.org

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Research Interests

Acute myelogenous leukemia; T-cell acute lymphoblastic leukemia; severe congenital neutropenia; hematopoiesis; myelopoiesis; lineage decision; transcription factor

Visit the Grimes Lab.

Dr. Grimes has a broad background in hematopoiesis, molecular biology, and molecular oncology including modeling of hematopoiesis, myelopoiesis and leukemia. His work on the Growth factor independent-1 (Gfi1) transcriptional repressor protein has spanned the initial identification of Gfi1 in a model of leukemia and the role of Gfi1 in normal myeloid biology, to the identification of GFI1 mutations in patients with severe congenital neutropenia (SCN) and non-immune chronic idiopathic neutropenia of adults (NI-CINA). His work utilizes Gfi1 as a molecular probe to understand both normal myeloid development and innate immune action, as well as marrow failure and transformation.

Education and Training

PhD: Immunology and Molecular Pathology, University of Florida, Gainesville, FL.

Postdoctoral Fellow: Fox Chase Cancer Center.

View PubMed Publications

Olsson A, Venkatasubramanian M, Chaudhri VK, Aronow BJ, Salomonis N, Singh H, Grimes HL. Single-cell analysis of mixed-lineage states leading to a binary cell fate choice. Nature. 2016 Aug 31.

Meyer SE, Qin T, Muench DE, Masuda K, Venkatasubramanian M, Orr E, Suarez L, Gore SD, Delwel R, Paietta E, Tallman MS, Fernandez H, Melnick A, Le Beau MM, Kogan S, Salomonis N, Figueroa ME, Grimes HL. DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia. Cancer Discovery. 2016; May;6(5):501-15.

Muench DE, Grimes HL. Transcriptional Control of Stem and Progenitor Potential. Curr Stem Cell Rep. 2015 Sep;1(3):139-150.

Nayak RC, Trump LR, Aronow BJ, Myers K, Mehta P, Kalfa T, Wellendorf AM, Valencia CA, Paddison PJ, Horwitz MS, Grimes HL#, Lutzko C#, Cancelas JA#. Pathogenesis of ELANE-mutant severe neutropenia revealed by induced pluripotent stem cells. J Clin Invest. 2015 Aug 3;125(8):3103-16. # shared corresponding author.

Cumaraswamy AA, Lewis AM, Geletu M, Todic A, Diaz DB, Cheng XR, Brown CE, Laister RC, Muench D, Kerman K, Grimes HL, Minden MD, Gunning PT. Nanomolar-Potency Small Molecule Inhibitor of STAT5 Protein. ACS Med Chem Lett. 2014 Sep 19;5(11):1202-1206.

Velu CS, Chaubey A, Phelan JD, Horman SR, Wunderlich M, Guzman ML, Jegga AG, Zeleznik-Le NJ, Chen J, Mulloy JC, Cancelas JA, Jordan CT, Aronow BJ, Marcucci G, Bhat B, Gebelein B, Grimes HL. Therapeutic antagonists of microRNAs deplete leukemia-initiating cell activity. J Clin Invest. 2014 Jan;124(1):222-36.

Phelan JD, Saba AI, Olsson A, Zeng H, Kosan C, Messer MS, Hildeman D, Aronow B, Möröy T, Grimes HL. Growth factor independent-1 maintains Notch1-dependent transcriptional programming of lymphoid precursors. PLoS Genetics. 2013;9(9):e1003713.

Khandanpour C*, Phelan JD*, Vassen L, Schutte J, Chen R, Horman SR, Gaudreau MC, Krongold J, Zhu J, Paul WE, Duhrsen U, Gottgens B, Grimes HL# Moroy T#. Growth factor independence 1 (Gfi1) antagonizes a p53-induced DNA damage response pathway in lymphoblastic leukemia. Cancer Cell. 2013 Feb 11;23(2):200-14. * equal first author, # shared corresponding author.

Developing Novel STAT5 Protein Inhibitors for treatment of leukemias. Principal Investigator. National Cancer Institute. Sept 2014–Sept 2017. R21CA186945.

MicroRNA in Acute Myeloid Leukemia. Principal Investigator. National Cancer Institute. Jul 2011–Apr 2017. R01CA159845.

Mechanisms of granulocyte homeostasis. Principal Investigator. National Heart Lung and Blood Institute. Sept 2015–Sept 2019. R01HL122661.

A rapid spontaneous murine model of CN-AML. Principal Investigator. National Cancer Institute. Jul 2016-Jun 2019. R01CA196658.

A photo of John Harley.

John B. Harley, MD, PhD Director, Center for Autoimmune Genomics and Etiology (CAGE)

John B. Harley, MD, PhD, is a rheumatologist and biochemist with special clinical and research interests in the genetic etiology of inflammatory diseases. His experimental focus is the many genetic effects and environmental causes of systemic lupus erythematosus (SLE) and related inflammatory diseases. Through this work, nearly 50 genes are known and Epstein Barr virus has been identified to trigger the systemic autoimmunity of lupus. Dr. Harley also builds infrastructure with which to do high throughput genotyping, expression analysis, and epigenetics, which he makes available to his colleagues from around the world. In recent experiments, Dr. Harley organized the logistics of managing >18,000 subjects at >30,000 genetic markers, 3200 subjects at 1.2 million markers, and 10,000 subjects at 196,000 markers. Dr. Harley is committed to all of the steps between association detection through replication and toward identifying the possible functional genetic variants and to pursuing their biology.

513-803-3665 john.harley@cchmc.org

A photo of John Harley.

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John B. Harley, MD, PhD

Director, Center for Autoimmune Genomics and Etiology (CAGE)

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-3665

Email john.harley@cchmc.org

View PubMed Publications

Cobb BL, Fei Y, Jonsson R, Bolstad AI, Brun JG, Rischmueller M, Lester SE, Witte T, Illei G, Brennan M, Bowman S, Moser KL, Harley JB, Sawalha AH. Genetic association between methyl-CpG binding protein 2 (MECP2) and primary Sjögren’s syndrome. Ann Rheum Dis. 2010; 69(9): 1731-2.

Kim-Howard X, Maiti AK, Anaya J-M, Bruner GR, Brown E, Merrill JT, Edberg JC, Petri MA, Reveille JD, Ramsey-Goldman R, Alarcon GS, Vyse TJ, Gilkeson G, Kimberly RP, James JA, Guthridge JM, Harley JB, Nath SK. ITGAM coding variant (rs1143679) influences the risk of renal disease, discoid rash, and immunologic manifestations in lupus patients with European ancestry. Ann Rheum Dis. 2010.

Javierre BM, Fernandez AF, Richter J, Al-Shahrour F, Martin-Subero JI, Rodriguez-Ubreva J, Berdasco M, Fraga MF, O'Hanlon TP, Rider LG, Jacinto FV, Lopez-Longo FJ, Dopazo J, Forn M, Peinado MA, Carreno L, Sawalha AH, Harley JB, Siebert R, Esteller M, Miller FW, Ballestar E. Changes in the pattern of DNA methylation associate with twin discordance in systemic lupus erythematosus. Genome Res. 2010; 20(2):170-179.

Harley JB, James JA. Everyone comes from somewhere: systemic lupus erythematosus and Epstein-Barr virus, induction of host interferon (INF) and humoral anti-EBNA1 immunity. Arthritis Rheum. 2010.

Bronson PG, Komorowski LK, Ramsay PP, May SL, Noble J, Lane JA, Thomson G, Claas FH, Seldin MF, Kelly JA, Harley JB, Moser KL, Gaffney PM, Behrens T, Criswell LA, Barcellos LF. Analysis of maternal-offspring HLA compatibility, parent-of-origin and noninherited effects for HLA-DRB1 in systemic lupus erythematosus. Arthritis Rheum. 2010.

Heinlen LD, McClain MT, Ritterhouse LL, Bruner BF, Edgerton CC, Keith MP, James JA, Harley JB. 60kD Ro and nRNP A frequently initiate human lupus autoimmunity. PLoS ONE. 2010 5(3):e9599.

Sammalisto S, Hiekkalinna T, Schwander K, Kardia S, Weder AB, Rodriquez BL, Doria A, Kelly JA, Bruner GR, Harley JB, Redline S, Larkin EK, Patel SR, Ewan AJ, Weber JL, Perola M, Peltonen L. Genome-wide linkage screen for stature and body mass index in 3.032 families: evidence for sex-and population-specific genetic effects. Eur J Hum Genet. 2009 Jan 1;17(2):258-266.

Poole BD, Templeton AK, Guthridge JM, Brown EJ, Harley JB, James JA. Aberrant Epstein-Barr viral infection in systemic lupus erythematosus. Autoimmun Rev. 2009 Feb;8(4):337-42.

Poole BD, Schneider RI, Guthridge JM, Velte CA, Reichlin M, Harley JB, James JA. Early targets of nuclear RNP humoral autoimmunity in human systemic lupus erythematosus. Arthritis Rheum. 2009 Feb 26; 60(3):848-859.

Han S, Kim-Howard X, Deshmukh H, Kamatani Y, Viswanathan P, Guthridge JM, Thomas K, Kaufman KM, Ojwang J, Rojas-Villarraga A, Baca V, Orozco L, Rhodes B, Choi CB, Gregersen PK, Merrill JT, James JA, Gaffney PM, Moser KL, Jacob CO, Kimberly RP, Harley JB, Bae SC, Anaya JM, Alarcon-Riquelme ME, Matsuda K, Vyse TJ, Nath SK. Evaluation of imputation-based association in and around the Integrin-α-M (ITGAM) gene and replication of robust association between a non-synonymous functional variant within ITGAM and systemic lupus erythematosus (SLE). Hum Mol Genet. 2009 Mar 15;18(6):1171-80.

A photo of David Haslam.

David B. Haslam, MD Director, Antimicrobial Stewardship Program

David B. Haslam, MD, is a pediatric infectious diseases physician who has research programs investigating the host and microbial factors that contribute to disease severity and outcome during Clostridium difficile infection. As medical director of the Antimicrobial Stewardship Program, he is initiating additional research programs on the interplay between antibiotic exposure, the host microbiome, and the molecular epidemiology of antimicrobial resistance.

513-803-1170 david.haslam@cchmc.org

A photo of David Haslam.

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David B. Haslam, MD

Director, Antimicrobial Stewardship Program

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-803-1170

Email david.haslam@cchmc.org

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Pediatric infectious diseases; host-microbial interactions; innate immunity

Education and Training

MD: University of Calgary, Calgary, Alberta, 1987.

Rotating Internship: McGill University, Montreal, Quebec, 1988.

Residency: University of Ottawa, Ottawa, Quebec, 1991.

Fellowship: Washington University School of Medicine, St. Louis, MO, 2005.

Certification: Pediatric Infectious Diseases, 1997.

View PubMed Publications

Cox JW, Ballweg RA, Taft DH, Velayutham P, Haslam DB, Porollo A. A fast and robust protocol for metataxonomic analysis using RNAseq data. Microbiome. 2017 Jan 19;5(1):7.

Andersen HM, Connolly NV, Bangar H, Staat M, Mortensen J, Deburger B, Haslam DB. Use of Shotgun Metagenome Sequencing to Detect Fecal Colonization with Multi-Drug Resistant Bacteria. J Clin Microbiol. 2016;54:1804-1813.

Zhou Y, Wylie KM, El Feghaly RE, Mihindukulasuriya KA, Elward A, Haslam DB, Storch GA, Weinstock GM. Metagenomic Approach for Identification of the Pathogens Associated with Diarrhea in Stool Specimens. J Clin Microbiol. 2016;54:368-375.

Haslam DB. Nonalcoholic steatohepatitis and the intestinal microbiota. Hepatology. 2016.

Forster CS, Courter J, Jackson EC, Mortensen JE, Haslam DB. Frequency of Multidrug-Resistant Organisms Cultured From Urine of Children Undergoing Clean Intermittent Catheterization. Journal of the Pediatric Infectious Diseases Society. 2016:piw056.

Goldstein SL, Mottes T, Simpson K, Barclay C, Muething S, Haslam DB, Kirkendall ES. A sustained quality improvement program reduces nephrotoxic medication-associated acute kidney injury. Kidney Int. 2016;90:212-221.

Ciricillo J, Haslam D, Blum S, Kim M-O, Liu C, Paulsen G, Courter J, Danziger-Isakov L. Frequency and risks associated with Clostridium difficile-associated diarrhea after pediatric solid organ transplantation: a single-center retrospective review. Transpl Infect Dis. 2016 Oct;18(5):706-713.

Dandoy CE, Haslam D, Lane A, Jodele S, Demmel K, El-Bietar J, Flesch L, Myers KC, Pate A, Rotz S, et al. Healthcare Burden, Risk Factors, and Outcomes of Mucosal Barrier Injury Laboratory-Confirmed Bloodstream Infections after Stem Cell Transplantation. Biol Blood Marrow Transplant. 2016.

El Feghaly R, Stauber J, Tarr PI, Haslam DB. Intestinal inflammatory biomarkers and outcome in pediatric Clostridium difficile infections. J Pediatr. 2013 Dec;163(6):1697-1704.

El Feghaly R, Stauber J, Deych E, Gonzales C, Tarr PI, Haslam DB. Markers of intestinal Inflammation, not bacterial burden, correlate with clinical outcomes in Clostridium difficile infection. Clin Infect Dis. 2013;56(12):1713-21.

Shotgun metagenomic sequencing to detect colonization, invasion, and transmission of multidrug-resistant organisms. Principal Investigator. Centers for Disease Control and Prevention.

Fecal metagenomics as a tool to identify and mitigate risk of bloodstream infection in high risk children. Principal Investigator. Center for Pediatric Genomics, Cincinnati Children’s Hospital Medical Center. Jan 2016-Dec 2016.

A photo of Andrew Herr.

Andrew B. Herr, PhD Director of Admissions, Immunology Graduate Program

Andrew B. Herr, PhD, studies protein-protein interactions involved in immune receptor signaling and bacterial pathogenesis. His lab uses X-ray crystallography to solve the atomic structures of proteins along with techniques of biophysical chemistry to understand their interactions in solution. The goal is to understand the molecular basis for autoimmune responses and recurrent bacterial infections, and to develop new therapeutic applications.
Visit the Herr Lab.

513-803-7490 andrew.herr@cchmc.org

A photo of Andrew Herr.

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Andrew B. Herr, PhD

Director of Admissions, Immunology Graduate Program

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-803-7490

Email andrew.herr@cchmc.org

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Research Interests

Structural biology and biophysics of antibodies; immune receptors; bacterial surface proteins

Visit the Herr Lab.

Andrew Herr, PhD, is an associate professor in the Division of Immunobiology and Center for Systems Immunology, with an affiliate appointment in the Division of Infectious Diseases at Cincinnati Children's within the UC Department of Pediatrics. Dr. Herr completed his thesis work in molecular biophysics from Washington University in St. Louis, and completed his postdoctoral work in structural immunology at the California Institute of Technology as a Damon Runyon Research Fellow. He was recruited to the University of Cincinnati College of Medicine as an Ohio Eminent Scholar in Structural Biology before moving to Cincinnati Children’s Hospital.

Dr. Herr solved the first structure of a human IgA1 antibody bound to its cognate Fc receptor while at Caltech, and his lab has continued to study antibodies and immune receptors implicated in autoimmune diseases. In addition, the lab is studying a family of related collagen-specific immune receptors such as glycoprotein VI, which activates platelets upon exposure to fibrous collagen. The Herr lab also studies mechanisms of bacterial pathogenesis. Specifically, they discovered the zinc-dependent mechanism of intercellular adhesion in bacterial biofilms formed by Staphylococcus epidermidis and S. aureus. Biofilms are specialized bacterial colonies that are highly resistant to antibiotics and immune responses, so developing novel therapies to prevent biofilm formation is of high importance.

Before joining the faculty at Cincinnati Children's within the University of Cincinnati College of Medicine, Dr. Herr was an Ohio Eminent Scholar in Structural Biology at the University of Cincinnati College of Medicine and served as an associate director of the Cincinnati Medical Scientist (MD/PhD) Training Program. Dr. Herr received the 2014 Emerging Entrepreneurial Achievement Faculty Award from UC for his work to commercialize a novel anti-infective therapy based on his lab’s research.

Education and Training

BA: Oral Roberts University, Tulsa, OK, 1993.

PhD: Washington University Medical School, St. Louis, MO, 1999.

Postdoc: California Institute of Technology, Pasadena, CA, 2003.

View PubMed Publications

Yarawsky AE, English LR, Whitten ST, Herr AB. The Proline/Glycine-Rich Region of the biofilm adhesion protein Aap forms an extended stalk that resists compaction. Journal of Molecular Biology. 2017;426:261-279.

Shelton CL, Conrady DG, Herr AB. Functional consequences of B-repeat sequence variation in the Staphylococcal biofilm protein Aap: Deciphering the assembly code. Biochemical Journal. 2017;474:427-443.

Zhou L, Hinerman JM, Blaszczyk M, Miller JLC, Conrady DG, Barrow AD, Chirgadze DY, Bihan D, Farndale RW, Herr AB. Structural basis for collagen recognition by the immune receptor OSCAR. Blood. 2016;127:529-537.

Chaton CT, Herr AB. Elucidating complicated assembling systems in biology using size-and-shape analysis of sedimentation velocity data. Methods in Enzymology: Analytical Ultracentrifugation. 2015;562:187-204.

Strait RT, Posgai MT, Mahler A, Barasa N, Jacob CO, Köhl J, Ehlers M, Stringer K, Shanmukappa SK, Witte D, Hossain MM, Khodoun M, Herr AB, Finkelman FD. IgG1 protects against renal disease in a mouse model of cryoglobulinemia. Nature. 2015;517:501-504.

Li X, Shu C, Yi G, Chaton CT, Shelton CL, Diao J, Zuo X, Kao CC, Herr AB, Li P. Cyclic GMP-AMP synthase is activated by double-stranded DNA-induced oligomerization. Immunity. 2013 Dec 12;39(6):1019-31.

Conrady DG, Wilson JJ, Herr AB. Structural basis for Zn2+-dependent intercellular adhesion in staphylococcal biofilms. Proc Natl Acad Sci U S A. 2013 Jan 15;110(3):E202-11.

Conrady DG, Brescia CC, Horii K, Weiss AA, Hassett DJ, Herr AB. A zinc-dependent adhesion module is responsible for intercellular adhesion in staphylococcal biofilms. Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19456-61.

Horii K, Kahn ML, Herr AB. Structural basis for platelet collagen responses by the immune-type receptor glycoprotein VI. Blood. 2006 Aug 1;108(3):936-42.

Herr, AB, ER Ballister, and PJ Bjorkman. Insights into IgA-mediated immune responses from the crystal structures of human FcaRI and its complex with IgA1-Fc. Nature. 2003 Jun 5;423(6940):614-20.

A photo of Gurjit Khurana Hershey.

Gurjit (Neeru) Khurana Hershey, MD, PhD Director, Division of Asthma Research

Gurjit (Neeru) Khurana Hershey, MD, PhD, is the principal investigator of a federally funded Asthma and Allergic Diseases Cooperative Research Center which supports, in part, the asthma and allergy-based Greater Cincinnati Pediatric Clinic Repository. She also focuses on elucidating the genetic and environmental factors that contribute to the development of asthma and eczema.

Visit the Khurana Hershey Lab.

513-636-7054 gurjit.hershey@cchmc.org

A photo of Gurjit Khurana Hershey.

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Gurjit (Neeru) Khurana Hershey, MD, PhD

Director, Division of Asthma Research

Co-Director, Office of Pediatric Clinical Fellowships

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-7054

Fax 513-636-1657

Email gurjit.hershey@cchmc.org

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Clinical & Research Interests

Clinical

Asthma; allergic rhinitis; food allergy; urticaria

Research

Genetics of allergy and asthma; cytokines; signaling pathways

Visit the Khurana Hershey Lab.

Gurjit Khurana Hershey, MD, PhD, received a BS degree from the University of Iowa, and MD and PhD degrees from Washington University School of Medicine. After completing pediatric residency and an allergy/immunology fellowship at St. Louis Children’s Hospital, Dr. Khurana Hershey joined the faculty at Cincinnati Children’s Hospital Medical Center within the University of Cincinnati College of Medicine. She now directs the Division of Asthma Research at Cincinnati Children’s Hospital Medical Center and is the director of the Medical Scientist Training Program at the University of Cincinnati College of Medicine.

In addition to her clinical duties, Dr. Khurana Hershey directs an NIH-funded research program focused on the genetics and genomics of allergic inflammation with a focus on cytokines and signal transduction. Her research has been continuously funded for over fifteen years. She is the principal investigator of an NIH-funded Asthma and Allergic Diseases Cooperative Research Center (AADCRC), and is also the PI of the Inner City Asthma Consortium, an NIH funded subcontract. She is the PI of the UC T32 MSTP training grant. In addition to her research contributions, she is an outstanding clinician and teacher/mentor. Several of her trainees now hold academic faculty positions. She is the recipient of the 2013 Cincinnati Children’s Educational Achievement Award.

Dr. Khurana Hershey is a fellow of the American Pediatric Society and the American Academy of Allergy, Asthma and Immunology. She serves on the Executive Council of the American Academy of Asthma, Allergy and Immunology Program Committee, is the chair of the Grant Review Committee and appointed vice chair of the Basic and Immunology Interest Section. She is a member of the Editorial Board of the Journal of Allergy and Clinical Immunology. She was recently named One of the Five Leading Women in Healthcare in the Greater Cincinnati Metropolitan Area, and Outstanding Woman at Cincinnati Children’s Hospital Medical Center.

Education and Training

BS: University of Iowa, Iowa City, IA, 1985.

PhD: Washington University School of Medicine, St. Louis, MO, 1990.

MD: Washington University School of Medicine, St. Louis, MO, 1992.

Residency: St. Louis Children's Hospital, St. Louis, MO, 1992-1995.

Fellowship: St. Louis Children's Hospital, St. Louis, MO, 1995-1997.

Board Certification: American Board of Pediatrics, 2009 - Present.

Board Certification: American Board of Allergy and Immunology, 2008 - Present.

View PubMed Publications

Biagini Myers JM, Martin LJ, Butsch Kovacic M, Mersha TB, He H, Pilipenko V, Lindsey MA, Ericksen MB, Bernstein DI, LeMasters GK, Lockey JE, Khurana Hershey GK. Epistasis between serine protease inhibitor Kazal-type 5 (SPINK5) and thymic stromal lymphopoietin (TSLP) genes contributes to childhood asthma. J Allergy Clin Immunol. 2014 May 13. pii: S0091-6749(14)00520-X.

Wood RA, Togias A, Wildfire J, Visness CM, Matsui EC, Gruchalla R, Hershey G, Liu AH, O’Connor GT, Pongracic JA, Zoratti E, Little F, Granada M, Kennedy S, Durham SR, Shamji MH, Busse WW. Development of cockroach immunotherapy by the Inner-City Asthma Consortium. J Allergy Clin Immunol. 2014 Mar;133(3)846-52.

Zhang Z, Xiao C, Gibson AM, Bass SA, Khurana Hershey GK. EGFR signaling blunts allergen-induced IL-6 production and Th17 responses in the skin and attenuates development and relapse of atopic dermatitis. J Immunol. 2014 Feb 1:192(3):859-66.

Kinker KG, Gibson AM, Bass SA, Day BP, Deng, J, Medvedovic M, Figueroa JA, Hershey GK, Chen W. Overexpression of dimethylarginine dimethylaminohydrolase 1 attenuates airway inflammation in a mouse model of asthma. PloS One. 2014 Jan 10;9 (1):e85148.

Acciani TH, Brandt EB, Khurana Hershey GK, Le Cras TD. Diesel exhaust particle exposure increases severity of allergic asthma in young mice and children. Clin Exp Allergy. 2013 Dec;43(12):1406-18.

Brandt EB, Kovacic MB, Lee GB, Gibson AM, Acciani TH, Le Cras TD, Budelsky AL, Khurana Hershey GK. Diesel exhaust particle induction of IL17A contributes to severe asthma. J Allergy Clin Immunol. 2013 Nov:132(5);1194-1204.

Brandt EB, Gibson AM, Bass S, Khurana Hershey GK. Exacerbation of Allergen-Induced Eczema in TLR4- and TRIF-Deficient Mice. J Immunol. 2013 Oct 1;191(7):3519-25.

Chen W, Sivaprasad U, Gibson AM, Ericksen MB, Cunningham CM, Bass SA, Kinker KG, Finkelman FD, Wills-Karp M, Khurana Hershey GK. IL-13 receptor α2 contributes to development of experimental allergic asthma. J Allergy Clin Immunol. 2013 Oct;132(4):951-958.

Lee GB, Brandt EB, Xiao C, Gibson AM, Le Cras TD, Brown LA, Fitzpatrick AM, Khurana Hershey GK. Diesel exhaust particles induce cysteine oxidation and S-glutathionylation in house dust mite induced murine asthma. PLoS One. 2013;8(3):e60632.

Mintz-Cole RA, Brandt EB, Bass SA, Gibson AM, Reponen T, Khurana Hershey GK. Surface availability of beta-glucans is critical determinant of host immune response to C. cladosporioides J Allergy Clin Immunol. 2013 Jul;132(1):159-69.

A photo of David Hildeman.

David A. Hildeman, PhD Director, Immunology Graduate Program

David A. Hildeman, PhD, explores the molecular factors that control the decision between tolerance and immunity within T lymphocytes. Using genetic mouse models, viruses, and MHC tetrameric reagents, the lab is focused on the molecular regulation of antigen-specific T cell responses. Dr. Hildeman is also the current director of the Immunology Graduate Program.
Visit the Hildeman Lab.

513-636-3923 david.hildeman@cchmc.org

A photo of David Hildeman.

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David A. Hildeman, PhD

Director, Immunology Graduate Program

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-3923

Fax 513-636-5355

Email david.hildeman@cchmc.org

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Clinical & Research Interests

Clinical

T cells; autoimmunity; sex differences in immune responses; apoptosis

Research

Molecular factors that control the decision between tolerance and immunity within T lymphocytes; staphylococcal enterotoxins, recombinant vaccinia viruses, lymphocytic choriomeningitis virus and MHC tetrameric reagents; antigen -specific T cell responses; tolerance centers on regulation of mechanisms that control the survival and death of activated T cells in vivo, namely Bcl-2 and its antagonist Bim; manipulation and regulation of antigen-specific T cell responses via novel vaccine strategies to either induce tolerance or enhance immunity; mechanisms underlying sex-based differences in T cell responses and how these differences relate to autoimmune disease.
Visit the Hildeman Lab.

Education and Training

PhD: University of Wisconsin-Madison, Madison, Wisconsin, 1997.

View PubMed Publications

Chae HD, Siefring JE, Hildeman DA, Gu Y, Williams DA. RhoH regulates subcellular localization of ZAP-70 and Lck in T cell receptor signaling. PLoS One. 2010 Nov 12;5(11):e13970.

Chougnet CA, Tripathi P, Lages CS, Raynor J, Sholl A, Fink P, Plas DR, Hildeman DA. A major role for Bim in regulatory T cell homeostasis. J Immunol. 2011 Jan 1;186(1):156-63.

Guo F, Hildeman D, Tripathi P, Velu CS, Grimes HL, Zheng Y. Coordination of IL-7 receptor and T-cell receptor signaling by cell-division cycle 42 in T-cell homeostasis. Proc Natl Acad Sci U S A. 2010 Oct 26;107(43):18505-10.

Kasten KR, Prakash PS, Unsinger J, Goetzman HS, England LG, Cave CM, Seitz AP, Mazuski CN, Zhou TT, Morre M, Hotchkiss RS, Hildeman DA, Caldwell CC. Interleukin-7 (IL-7) treatment accelerates neutrophil recruitment through gamma delta T-cell IL-17 production in a murine model of sepsis. Infect Immun. 2010 Nov;78(11):4714-22.

Tripathi P, Kurtulus S, Wojciechowski S, Sholl A, Hoebe K, Morris SC, Finkelman FD, Grimes HL, Hildeman DA. STAT5 is critical to maintain effector CD8+ T cell responses. J Immunol. 2010 Aug 15;185(4):2116-24.

Kurtulus S, Tripathi P, Opferman JT, Hildeman DA. Contracting the 'mus cells' -- does down-sizing suit us for diving into the memory pool? Immunol Rev. 2010 Jul;236:54-67. Review.

Lin AA, Wojciechowski SE, Hildeman DA. Androgens suppress antigen-specific T cell responses and IFN-γ production during intracranial LCMV infection. J Neuroimmunol. 2010 Sep 14;226(1-2):8-19.

Kasten KR, Tschöp J, Goetzman HS, England LG, Dattilo JR, Cave CM, Seitz AP, Hildeman DA, Caldwell CC. T-cell activation differentially mediates the host response to sepsis. Shock. 2010 Oct;34(4):377-83.

Kasten KR, Tschöp J, Adediran SG, Hildeman DA, Caldwell CC. T cells are potent early mediators of the host response to sepsis. Shock. 2010 Oct;34(4):327-36. Review.

Madan R, Demircik F, Surianarayanan S, Allen JL, Divanovic S, Trompette A, Yogev N, Gu Y, Khodoun M, Hildeman D, Boespflug N, Fogolin MB, Gröbe L, Greweling M, Finkelman FD, Cardin R, Mohrs M, Müller W, Waisman A, Roers A, Karp CL. Nonredundant roles for B cell-derived IL-10 in immune counter-regulation. J Immunol. 2009 Aug 15;183(4):2312-20.

A photo of Shouxiong Huang.

Shouxiong Huang, PhD Member, Immunology Graduate Program

investigates the activation and function of innate-like T cells in responses to vitamin-like and lipid antigens using metabolomic and biological approaches. The goal is to discover novel structures and presentation mechanisms of antigens that induce protective T cell responses and ultimately facilitate controlling immune disorders and environmental exposure.

513-558-7572 shouxiong.huang@uc.edu

A photo of Shouxiong Huang.

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Shouxiong Huang, PhD

Member, Immunology Graduate Program

Academic Affiliations

Assistant Professor, UC Department of Environmental Health

Phone 513-558-7572

Email shouxiong.huang@uc.edu

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Dr. Huang’s studies have been focused on the activation and function of T cells in infectious and inflammatory diseases. During his postdoctoral training with Ted Hansen at Washington University, he started understanding the activation mechanism of innate-like T cells, specifically the mucosal-associated invariant T cells (MAIT) that are restricted by MHC class I like molecule MR1. He generated three major findings including the requirement of an antigen for MAIT cell activation (J Biol Chem, 2005), endocytic pathway of MAIT cell antigen loading (J Exp Med, 2008), and innate-like recognition of MR1 antigen complex by semi-invariant MAIT T cell receptor (PNAS, 2009). These findings supported the hypothesis that MAIT cells bear a rapid innate-like activation mechanism able to uniquely regulate mucosal diseases (Nat Immunol, 2007 review) and further inspired the discovery of MAIT cell protection against mycobacterial infection (Nat Immunol, 2010). As the lipid-responding T cells also show similar innate-like activation features, Dr. Huang’s additional training with Branch Moody at Harvard Medical School helped him establish a metabolomic platform and its applications to the antigens presented by MHC class I like CD1 proteins for the activation of lipid-responding T cells. These studies firstly revealed that the CD1b scaffold lipid diacylglycerol facilitates the presentation of the antigen mycobacterial glucose monomycolate to activate T cells from human tuberculosis (PNAS, 2011). Further collaboration using his metabolomic platform has discovered that mycobacterial and host lipid antigens were able to activate CD1c and CD1a-restricted T cells (J Exp Med, 2013, Nature Immunol, 2013).

Dr. Huang is extending the studies on the activation mechanisms and antigen structures of innate-like T cells particularly to the settings of mycobacterial infection, gut inflammation, and environmental exposure.

Education and Training

BS: Beijing University of Chinese Medicine, 1993.

PhD: The Ohio State University, 2003.

Postdoc: Washington University in St. Louis, 2003-2009.

Postdoc: Harvard Medical School, 2009-2011.

de Jong A, Cheng TY, Huang S, Gras S, Birkinshaw R, Kasmar A, van Rhijn I, Peña-Cruz V, Ruan DT, Altman JD, Rossjohn J, Moody DB. CD1a autoreactive T cells recognize natural skin oils that function as headless antigens. Nature Immunology. 2014;15(2):177-85.

Ly D, Kasmar AG, Cheng TY, de Jong A, Huang S, Roy S, Bhatt A, van Summeren RP, Altman JD, Jacobs Jr WR, Adams EJ, Minnaard AJ, Porcelli SA, Moody DB. CD1c tetramers detect ex vivo T cell responses to processed Mycobacterium phosphomycoketide antigens. Journal of Experimental Medicine. 2013;210(4):729-41.

Young MH, U'Ren L, Huang S, Mallevaey T, Scott-Browne J, Crawford F, Lantz O, Hansen TH, Kappler J, Marrack P, Gapin L. MAIT cell recognition of MR1 on bacterially infected and uninfected cells. PLOS ONE. 2013;8(1):e53789.

Huang S, Cheng TY, Young D, Layre E, Madigan C, Shires J, Cerundolo V, Altman JD, and Moody DB. Discovery of deoxyceramides and diacylglycerols as CD1b scaffold lipids among the diverse groove blocking lipids of the human CD1 system. Proc Natl Acad Sci USA. 2011;108(48):19335-19340.

Chua WJ, Yu L, Kim S, Myers N, Huang S, Fremont DH, Hansen TH. Endogenous MR1 is transiently expressed on the cell surface in a functional conformation capable of MAIT cell activation. J Immunol. 2011;186(8):4744-4750.

Le Bourhis L, Martin E, Péguillet I, Guihot A, Froux N, Coré M, Lévy E, Dusseaux M, Meyssonnier V, Premel V, Ngo C, Riteau B, Duban L, Robert D, Huang S, Rottman M, Soudais C, Lantz O. Antimicrobial activity of mucosal-associated invariant T cells. Nature Immunology. 2010;11(8):701-708.

Huang S, Martin E, Kim S, Yu L, Soudais C, Fremont DH, Lantz O, Hansen TH. MR1 antigen presentation to mucosal-associated invariant T cells was highly evolutionarily conserved. Proc Natl Acad Sci USA. 2009:106(20):8290-8295.

Huang S, Gilfillan S, Kim S, Thompson B, Wang X, Sant AJ, Fremont DH, Lantz O, and Hansen TH. MR1 uses an endocytic pathway to activate mucosal-associated invariant T cells. Journal of Experimental Medicine. 2008;205(5):1201-1211.

Hansen TH, Huang S, Arnold PL, Fremont DH. Patterns of nonclassical MHC antigen presentation (Review). Nature Immunology. 2007;8(6):563-568.

Huang S, Sahin O, Zhang Q. Infection induced antibodies against the major outer membrane protein of Campylobacter jejuni mainly recognize conformational epitopes. FEMS Microbiology Letters. 2007;272(7):137-143.

Shouxiong Huang. Antigen metabolomics for mucosal-associated invariant T cells in tuberculosis. Principal Investigator. National Institute of Allergy and Infectious Diseases (NIAID). Dec 2014-Nov 2016.

A photo of Vivian Hwa.

Vivian Hwa, PhD Basic Research Director, Cincinnati Center for Growth Disorders

Vivian Hwa, PhD, investigates the functional and cellular impacts of genetic defects identified in children with severe growth failure, who often present with a variety of co-morbidities, including immune deficiencies, insulin insensitivities, intellectual impairment, microcephaly. These pathophysiological mutations provide unique opportunities to delineate molecular mechanism(s) of actions and improve understanding of clinical phenotypes.
Visit the Dauber-Hwa Lab.

513-803-7337 vivian.hwa@cchmc.org

A photo of Vivian Hwa.

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Vivian Hwa, PhD

Basic Research Director, Cincinnati Center for Growth Disorders

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-803-7337

Email vivian.hwa@cchmc.org

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Research Interests

Visit the Dauber - Hwa Lab.

Education and Training

BS: University of Sydney, Sydney, Australia.

PhD: University of Illinois, Champaign-Urbana, IL.

View PubMed Publications

Kern SL, Guevara-Aguirre J, Andrew S, Geng J, Guevara C, Guevara-Aguirre M, Guo M, Oddoux C, Shen Y, Zurita A, Rosenfeld RG, Ostrer H, Hwa V, Dauber A. A novel variant in CDKN1C is associated with intrauterine growth restriction, short stature, and early-adulthood onset diabetes. J Clin Endocrinol Metab. 2014 Oct;99(10):E2117-22.

Feigerlova E, Swinyard M, Andrew SF, Derr MA, Farnsworth J, Rosenfeld RG, Hwa V. A novel GHR intronic variant c.266+83G>T, activates a cryptic 5’ splice site causing severe GHR deficiency and classical GH insensitivity syndrome. Horm Res Paediatr. 2013;80(6):397-405.

Varco-Merth B, Feigerlová E, Shinde U, Rosenfeld RG, Hwa V, Rotwein P. Severe growth deficiency is associated with STAT5b mutations that disrupt protein folding and activity. Mol Endocrinol. 2013 Jan;27(1):150-61.

Dauber A, LaFranchi SH, Maliga Z, Lui JC, Moon JE, McDeed C, Henke K, Zonana J, Kingman GA, Pers TH, Baron J, Rosenfeld RG, Hirschhorn JN, Harris MP, Hwa V. Novel Microcephalic Primordial Dwarfism Disorder Associated with Variants in the Centrosomal Protein Ninein. J Clin Endocrinol Metab. 2012 Nov;97(11):E2140-51.

Scalia PA, Martinez AS, Feigerlova E, Bezrodnik L, Gaillard MI, Di Giovanni D, Ballerini MG, Jasper HG, Heinrich JJ, Fang P, Domené HM, Rosenfeld RG, Hwa V. A novel missense mutation in the SH2 domain of the STAT5B gene results in a transcriptionally inactive STAT5b associated with severe IGF-I deficiency, immune dysfunction, and lack of pulmonary disease. J Clin Endocrinol Metab. 2012 May;97(5):E830-9.

Derr MA, Aisenberg J, Fang P, Tenenbaum-Rakover Y, Rosenfeld RG, Hwa V. The growth hormone receptor (GHR) c.899dupC mutation functions as a dominant negative: insights into the pathophysiology of intracellular GHR defects. J Clin Endocrinol Metab. 2011 Nov;96(11):E1896-904.

Fang P, Kofoed EM, Little BM, Ross RJM, Frank, SJ, Hwa V, Rosenfeld RG. A mutant STAT5b, associated with growth hormone insensitivity and IGF-I deficiency, cannot function as a signal transducer or transcription factor. J Clin Endocrinol Metab. 2006 Apr; 91(4):1526-34.

Hwa V, Little B, Adiyaman P, Kofoed E, Pratt KL, Ocal G, Berberoglu M, Rosenfeld RG. Severe growth hormone insensitivity resulting from total absence of signal transducer and activator of transcription 5b. J Clin Endocrinol Metab. 2005 Jul;90(7):4260-6.

Hwa V, Little B, Kofoed EM, Rosenfeld RG. Transcriptional regulation of insulin-like growth factor-I (IGF-I) by interferon-gamma (IFN-γ) requires STAT-5b. J Biol Chem. 2004 Jan 23;279(4):2728-36.

Kofoed EM*, Hwa V*, Little B, Woods KA, Buckway CK, Tsubaki J, Pratt KL, Bezrodnik L, Jasper H, Tepper A, Heinrich JJ, Rosenfeld RG. Growth hormone insensitivity associated with a STAT5b mutation. N Engl J Med. 2003 Sep 18:349(12):1139-47. *co-first authors

A photo of Michael Jordan.

Michael B. Jordan, MD Member, Division of Bone Marrow Transplantation and Immune Deficiency

Michael B. Jordan, MD, specializes in caring for children with histiocytic disorders, primary immune deficiencies, or who are undergoing bone marrow transplantation. His laboratory focuses on understanding effector T cell function, immune regulation, and the pathogenesis of hemophagocytic lymphohistiocytosis. He is also conducting preclinical scientific studies in addition to a translational clinical trial.

513-636-1773 michael.jordan@cchmc.org

A photo of Theodosia A. Kalfa.

Theodosia A. Kalfa, MD, PhD Co-Director, Erythrocyte Diagnostic Laboratory

Theodosia A. Kalfa, MD, PhD, focuses on the study of intracellular signals in erythropoiesis and mature red blood cells, specifically the signals conducted by Rho GTPases regulating terminal erythroid maturation and enucleation. Her lab also studies the role of Rac GTPases in generation of reactive oxygen species (ROS) within red blood cells from patients and animal models with sickle-cell disease along with the signaling mechanisms and consequences of increased ROS in sickle cells.
Visit the Kalfa Lab.

513-636-0989 theodosia.kalfa@cchmc.org

A photo of Theodosia A. Kalfa.

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Theodosia A. Kalfa, MD, PhD

Co-Director, Erythrocyte Diagnostic Laboratory

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-636-0989

Fax 513-636-3549

Email theodosia.kalfa@cchmc.org

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Research Interests

Signaling in erythrocytes; erythropoiesis; sickle cell disease; reactive oxygen species

Visit the Kalfa Lab.

Education and Training

MD: Aristotle University Medical School, Thessaloniki, Greece, 1990.

PhD: Aristotle University Medical School, Thessaloniki, Greece, 1997.

Residency: University Of North Carolina, Chapel Hill, NC, 1999.

Fellowship: Duke University Medical Center, Durham, NC, 2003.

Certification: Hematology / oncology, American Board of Pediatrics, 2004; Pediatrics, American Board of Pediatrics, 2000; ECFMG Certification, 1995.

Licenses: Full and unrestricted medical license (OH Medical Board), 2003-present; full and unrestricted license of medical practice in Greece, 1990-present.

View PubMed Publications

Rho GTPases in Terminal Erythroid Maturation. Principal Investigator. NIH/NHLBI. Sep 2012-Jun 2016. #1R01HL116352.

Cincinnati Center of Excellence in Hemoglobinopathies Research. Co-investigator. NIH/NHLBI. Aug 2013–May 2018. # U01 HL117709.

A photo of Jonathan Katz.

Jonathan D. Katz, PhD

Jonathan D. Katz, PhD, is working to understand the role that autoreactive T lymphocytes play in the Immunopathogenesis of type 1 diabetes, the most common pediatric autoimmune disease. Major focuses include defining: (a) the control of autoreactive T cells via central and peripheral tolerance; (b) the role NKT cells play in regulating autoreactive T cells; and (c) the role dendritic cells play in activating and regulating autoreactive T cells in type 1 diabetes.
Visit the Katz Lab.

513-636-5306 jonathan.katz@cchmc.org

A photo of Jonathan Katz.

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Jonathan D. Katz, PhD

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-5306

Fax 513-636-5355

Email jonathan.katz@cchmc.org

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Clinical & Research Interests

Clinical

T cells; MHC, beta cell death; islet antigens

Research

Immunology; autoimmunity; type 1 diabetes

Visit the Katz Lab.

Jonathan D. Katz, PhD, focuses on autoimmune diabetes research. Autoimmune diabetes, also known as type 1 diabetes (T1D), is the most common pediatric autoimmune disease. Roughly 1/250 individuals develop T1D in the United States.There is currently no cure for T1D and the only treatment is daily exogenous insulin replacement therapy. Many T1D patients eventually develop secondary complications, such as hearth disease, blindness, peripheral neuropathy and renal failure.

Dr. Katz's work focuses on the role that autoreactive T lymphocytes play in the disease process. His lab is interested in (1) the control of autoreactive T cells via central and peripheral tolerance, (2) the role NKT cells play in regulating autoreactive T cells, and (3) the role dendritic cells play in activating and regulating autoreactive T cells in T1D.

Most of his work uses the non-obese diabetic (NOD) mouse strain that spontaneously develops T1D with remarkable similarity to the T1D seen in human patients. The availability of the NOD strain has allowed the lab to take a modern, reductionist molecular and cellular immunology approach to understanding the mechanism(s) and genetics underlying T1D susceptibility and disease progression. Dr. Katz's lab makes extensive use of knockout, transgenic, regulated gene expression, targeted ablation, cell transfer and genomic studies the progression and regulation of T1D in the NOD mouse.

Education and Training

BS: University of California, Los Angeles, CA, 1984.

PhD: University of California, Los Angeles, CA, 1990.

Post-Doctoral Fellow: Université Louis Pasteur, Strasbourg, France, 1990-1995.

View PubMed Publications

Katz JD, Ondr JK, Opoka RJ, Garcia Z, Janssen EM. Cutting edge: merocytic dendritic cells break T cell tolerance to beta cell antigens in nonobese diabetic mouse diabetes. J Immunol. 2010 Aug 15;185(4):1999-2003.

Pang S, Zhang L, Wang H, Yi Z, Li L, Gao L, Zhao J, Tisch R, Katz JD, Wang B. CD8(+) T cells specific for beta cells encounter their cognate antigens in the islets of NOD mice. Eur J Immunol. 2009 Oct;39(10):2716-24.

Saxena V, Ondr JK, Magnusen AF, Munn DH, Katz JD. The countervailing actions of myeloid and plasmacytoid dendritic cells control autoimmune diabetes in the nonobese diabetic mouse. J Immunol. 2007 Oct 15;179(8):5041-53.

Wojciechowski S, Tripathi P, Bourdeau T, Acero L, Grimes HL, Katz JD, Finkelman FD, Hildeman DA. Bim/Bcl-2 balance is critical for maintaining naive and memory T cell homeostasis. J Exp Med. 2007 Jul 9;204(7):1665-75.

Cain JA, Smith JA, Ondr JK, Wang B, Katz JD. NKT cells and IFN-gamma establish the regulatory environment for the control of diabetogenic T cells in the nonobese diabetic mouse. J Immunol. 2006 Feb 1;176(3):1645-54.

Vukkadapu SS, Belli JM, Ishii K, Jegga AG, Hutton JJ, Aronow BJ, Katz JD. Dynamic interaction between T cell-mediated beta-cell damage and beta-cell repair in the run up to autoimmune diabetes of the NOD mouse. Physiol Genomics. 2005 Apr 14;21(2):201-11.

Hutton JJ, Jegga AG, Kong S, Gupta A, Ebert C, Williams S, Katz JD, Aronow BJ. Microarray and comparative genomics-based identification of genes and gene regulatory regions of the mouse immune system. BMC Genomics. 2004 Oct 25;5(1):82.

A photo of Kenneth M. Kaufman.

Kenneth M. Kaufman, PhD

Kenneth M. Kaufman, PhD, investigates the genetics of complex and rare disorders using genotyping and next-generation DNA technologies. The goal of his research is to identify the underling mechanisms and genetics that lead to complex diseases such as systemic lupus erythematosus.

513-803-5385 kenneth.kaufman@cchmc.org

A photo of Kenneth M. Kaufman.

High Res

Kenneth M. Kaufman, PhD

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-5385

Email kenneth.kaufman@cchmc.org

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Research Interests

Genetics; bio-informatics

A large portion of Dr. Kaufman's research career has been on the genetics of systemic lupus erythematsus. Their work has screened 10's of thousands of lupus cases and controls with millions of polymorphic markers. This work has resulted in the identification, replication and/or fine mapping of over 70 genetic associations with systemic lupus erythematsus.

Recently, they have taken advantage of next generation DNA sequencing to identify variants that directly cause disease. They have developed a number of bioinformatic pipelines that can be applied to any phenotype. These automated pipelines are part of the Cincinnati Analytical Suite for Sequencing Informatics (CASSI) which has been applied to more than 20 different diseases and provides a list of candidate causative variants that lead to disease.

Education and Training

PhD: University of South Carolina, Columbia, SC, 1991.

View PubMed Publications

Kottyan LC, Zoller EE, Bene J, Lu X, Kelly JA, Rupert AM, Lessard CJ, Vaughn SE, Marion M, Weirauch MT, Namjou B, Adler A, Rasmussen A, Glenn S, Montgomery CG, Hirschfield GM, Xie G, Coltescu C, Amos C, Li H, Ice JA, Nath SK, Mariette X, Bowman S; UK Primary Sjögren's Syndrome Registry, Rischmueller M, Lester S, Brun JG, Gøransson LG, Harboe E, Omdal R, Cunninghame-Graham DS, Vyse T, Miceli-Richard C, Brennan MT, Lessard JA, Wahren-Herlenius M, Kvarnström M, Illei GG, Witte T, Jonsson R, Eriksson P, Nordmark G, Ng WF; UK Primary Sjögren's Syndrome Registry, Anaya JM, Rhodus NL, Segal BM, Merrill JT, James JA, Guthridge JM, Scofield RH, Alarcon-Riquelme M, Bae SC, Boackle SA, Criswell LA, Gilkeson G, Kamen DL, Jacob CO, Kimberly R, Brown E, Edberg J, Alarcón GS, Reveille JD, Vilá LM, Petri M, Ramsey-Goldman R, Freedman BI, Niewold T, Stevens AM, Tsao BP, Ying J, Mayes MD, Gorlova OY, Wakeland W, Radstake T, Martin E, Martin J, Siminovitch K, Moser Sivils KL, Gaffney PM, Langefeld CD, Harley JB, Kaufman KM. The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share. Hum Mol Genet. 2015 Jan 15;24(2):582-96.

Kaufman KM, Linghu B, Szustakowski JD, Husami A, Yang F, Zhang K, Filipovich AH, Fall N, Harley JB, Nirmala NR, Grom AA. Whole-exome sequencing reveals overlap between macrophage activation syndrome in systemic juvenile idiopathic arthritis and familial hemophagocytic lymphohistiocytosis. Arthritis Rheumatol. 2014 Dec;66(12):3486-95.

Patel ZH, Kottyan LC, Lazaro S, Williams MS, Ledbetter DH, Tromp H, Rupert A, Kohram M, Wagner M, Husami A, Qian Y, Valencia CA, Zhang K, Hostetter MK, Harley JB, Kaufman KM. The struggle to find reliable results in exome sequencing data: filtering out Mendelian errors. Front Genet. 2014 Feb 12;5:16.

Kaufman KM, Zhao J, Kelly JA, Hughes T, Adler A, Sanchez E, Ojwang JO, Langefeld CD, Ziegler JT, Williams AH, Comeau ME, Marion MC, Glenn SB, Cantor RM, Grossman JM, Hahn BH, Song YW, Yu CY, James JA, Guthridge JM, Brown EE, Alarcón GS, Kimberly RP, Edberg JC, Ramsey-Goldman R, Petri MA, Reveille JD, Vilá LM, Anaya JM, Boackle SA, Stevens AM, Freedman BI, Criswell LA, Pons Estel BA; Argentine Collaborative Group, Lee JH, Lee JS, Chang DM, Scofield RH, Gilkeson GS, Merrill JT, Niewold TB, Vyse TJ, Bae SC, Alarcón-Riquelme ME; BIOLUPUS network, Jacob CO, Moser Sivils K, Gaffney PM, Harley JB, Sawalha AH, Tsao BP. Fine mapping of Xq28: both MECP2 and IRAK1 contribute to risk for systemic lupus erythematosus in multiple ancestral groups. Ann Rheum Dis. 2013 Mar;72(3):437-44.

International Consortium for Systemic Lupus Erythematosus Genetics (SLEGEN), Harley JB, Alarcón-Riquelme ME, Criswell LA, Jacob CO, Kimberly RP, Moser KL, Tsao BP, Vyse TJ, Langefeld CD, Nath SK, Guthridge JM, Cobb BL, Mirel DB, Marion MC, Williams AH, Divers J, Wang W, Frank SG, Namjou B, Gabriel SB, Lee AT, Gregersen PK, Behrens TW, Taylor KE, Fernando M, Zidovetzki R, Gaffney PM, Edberg JC, Rioux JD, Ojwang JO, James JA, Merrill JT, Gilkeson GS, Seldin MF, Yin H, Baechler EC, Li QZ, Wakeland EK, Bruner GR, Kaufman KM, Kelly JA. Genome-wide association scan in women with systemic lupus erythematosus identifies susceptibility variants in ITGAM, PXK, KIAA1542 and other loci. Nat Genet. 2008 Feb;40(2):204-10.

A photo of Raphael Kopan.

Raphael Kopan, PhD Director, Division of Developmental Biology

Raphael Kopan, PhD, and his lab have the long-term goal of organogenesis in vitro. They focus their efforts on Notch signaling as their lead into mechanistic understanding of tissue diversity using genetic engineering, embryology and single cell profiling. They interrogate the mouse embryo to address critical questions regarding the circuit logic of Notch signaling in mammalian organogenesis and its integration in larger signaling context.

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513-636-1299

A photo of Raphael Kopan.

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Raphael Kopan, PhD

Director, Division of Developmental Biology

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-1299

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Research Interests

Notch signaling; kidney organogenesis; skin organogenesis; TSLP signaling in cancer

Visit the Kopan Lab.

Raphael Kopan, PhD, who is a professor of developmental biology at Cincinnati Children's Hospital Medical Center within the University of Cincinnati College of Medicine, has carried out seminal work in the field of Notch biology. This work has, and continues to have, an enormous impact on our understanding of normal tissue development and renewal, Alzheimer's disease and cancer-related research. In deciphering the mode of Notch activation and demonstrating the use of inhibitors to modulate Notch activity, Dr. Kopan's work laid the groundwork for the therapeutic use of γ-secretase inhibitors in the treatment of cancers, currently in clinical trials. His current interests in organogenesis are focused on two modular organs - skin and kidney - in which his group is trying to understand how interplay among the same seven pathways results in activation of distant programs. Dr. Kopan's work has resulted in 120 scientific articles as of 2013. He is the co-inventor of one patent, and he has served on scientific advisory boards as well as being a consultant to the pharmaceutical industry.

Education and Training

BS, MsC: Department of Zoology, Tel-Aviv University, Israel.

PhD: Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL.

Post-doctoral training : The Fred Hutchinson Cancer Research Center, Seattle, WA.

View PubMed Publications

Chen S, Brunskill EW, Potter SS, Dexheimer PJ, Salomonis N, Aronow BJ, Hong CI, Zhang T, Kopan R. Intrinsic Age-Dependent Changes and Cell-Cell Contacts Regulate Nephron Progenitor Lifespan. Developmental Cell. 2015;35:49-62.

Hass MR, Liow HH, Chen X, Sharma A, Inoue YU, Inoue T, Reeb A, Martens A, Fulbright M, Raju S, Stevens M, Boyle S, Park JS, Weirauch MT, Brent MR, Kopan R. SpDamID: Marking DNA Bound by Protein Complexes Identifies Notch-Dimer Responsive Enhancers. Molecular Cell. 2015;9(4):685-697.

Demitrack ES, Gifford GB, Keeley TM, Carulli AJ, VanDussen KL, Thomas D, Giordano TJ, Liu Z, Kopan R, Samuelson LC. Notch signaling regulates gastric antral LGR5 stem cell function. EMBO J. 2015 Aug 12.

Liu Z, Brunskill E, Varnum-Finney B, Zhang C, Zhang A, Jay PY, Bernstein I, Morimoto M, Kopan R. The intracellular domains of Notch1 and 2 are functionally equivalent during development and carcinogenesis. Development. 2015;142:2452-2463.

Liu Z, Brunskill E, Boyle S, Chen S, Turkoz M, Guo Y, Grant R, Kopan R. Second-generation Notch1 activity-trap mouse line (N1IP::CreHI) provides a more comprehensive map of cells experiencing Notch1 activity. Development. 2015 Mar 15;142(6):1193-202.

Demehri S, Yockey LJ, Visness CM, Jaffee KF, Turkoz A, Wood RA, O'Connor GT, Kattan M, Gern JE, Gergen PJ, Holtzman M, Bloomberg G, Kopan R. Circulating TSLP associates with decreased wheezing in non-atopic preschool children: Data from the URECA birth cohort. Clin Exp Allergy. 2014 Jun;44(6):851-7.

Zhao ZQ, Huo FQ, Jeffry J, Hampton L, Demehri S, Kim S, Liu XY, Barry DM, Wan L, Liu ZC, Li H, Turkoz A, Ma K, Cornelius LA, Kopan R, Battey JF Jr, Zhong J, Chen ZF. Chronic itch development in sensory neurons requires BRAF signaling pathways. J Clin Invest. 2013 Nov;123(11):4769-80.

Chillakuri CR, Sheppard D, Ilagan MX, Holt LR, Abbott F, Liang S, Kopan R, Handford PA, Lea SM. Structural analysis uncovers lipid-binding properties of notch ligands. Cell Rep. 2013 Nov 27;5(4):861-7.

Boyle SC1, Liu Z, Kopan R. Notch signaling is required for the formation of mesangial cells from a stromal mesenchyme precursor during kidney development. Development. 2014 Jan;141(2):346-54.

Satpathy AT, Briseño CG, Lee JS, Ng D, Manieri NA, Kc W, Wu X, Thomas SR, Lee WL, Turkoz M, McDonald KG, Meredith MM, Song C, Guidos CJ, Newberry RD, Ouyang W, Murphy TL, Stappenbeck TS, Gommerman JL, Nussenzweig MC, Colonna M, Kopan R, Murphy KM. Notch2-dependent classical dendritic cells orchestrate intestinal immunity to attaching-and-effacing bacterial pathogens. Nat Immunol. 2013 Sep;14(9):937-48.

A photo of Leah Kottyan.

Leah C. Kottyan, PhD

Leah C. Kottyan, PhD, studies the molecular and immunological mechanisms driving the statistical association of genetic variants with systemic lupus erythematosus and eosinophilic esophagitis. The goal of her research is to refine the statistical analysis of genetic data while using analytical and biological tools to predict and confirm genetic variant-dependent differences that affect gene expression, cell function, and disease risk.

513-636-1316 leah.kottyan@cchmc.org

A photo of Leah Kottyan.

High Res

Leah C. Kottyan, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-1316

Email leah.kottyan@cchmc.org

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Research Interests

Genetic basis of lupus; genetic basis of eosinophilic esophagitis; immunological mechanisms mediating genetic association with disease

Visit the Kottyan Lab.

For the past decade, many geneticists have approached genetic analysis with the idea that they simply need to increase statistical power by enlarging the sample size (e.g. ~100,000 person height GWAS) and assess enough loci in order to find the “genes” associated with a disease. Unfortunately, clinicians can do relatively little with this type of correlative genetic information. Dr. Kottyan recently lead a genome-wide association analysis of eosinophilic esophagitis in which they went beyond the identification of nine new risk loci and identified the molecular, tissue-specific mechanisms through which genetic variants at the CAPN14 locus increase risk of disease.

During her post-doctoral fellowship, she optimized statistical modeling strategies using genetic data from large multi-ancestral cohorts to identify candidate genetic causal variants through complementary frequentist and Bayesian approaches. In genetic analysis, it is easy and even tempting to make a story out of a genetic variant that seems important. Using two types of statistical analyses on multiple cohorts of different ancestry helps to avoid the misplaced attribution of causality. Instead, Dr. Kottyan’s group develops a short list of variants that are most statistically likely to be causal before they start biological or functional analysis. Once identified, the group predicts and confirms biological phenotypes that are affected by the risk variants.

Education and Training

BA: Chemistry and Cell Biology, Huntingdon College, Montgomery, AL, 2005.

PhD: Immunobiology, University of Cincinnati, Cincinnati, OH, 2010.

View PubMed Publications

Lu X, Zoller EE, Weirauch M, Wu X, Namjou-Khales B, Williams A, Ziegler J, Comeau MR, Marion M, Glenn S, Adler A, Shen N, Nath SK, Stevens AM, Freedman BI, Tsao BP, Jacob CO, Kamen DL, Brown E, Gilkeson G, Alarcon GS, Reveille JD, Anaya JM, James JA, Sivils K, Criswell LA, Vila LM, Alarcon-Riquelme M, Petri M, Scofield RH, Kimberly R, Ramsey-Goldman R, Joo YB, Choi J, Bae SC, Boackle SA, Cunninghame-Graham DS, Vyse T, Guthridge JM, Gaffney PM, Langefeld CD, Kelly J, Greis K, Kaufman K, Harley JB, Kottyan L. Lupus risk-variant increases pSTAT1 binding and decreases ETS1 expression. American journal of human genetics. 2015.

Vaughn SE, Foley C, Lu X, Patel ZH, Zoller EE, Magnusen AF, Williams AH, Ziegler JT, Comeau ME, Marion MC, Glenn SB, Adler A, Shen N, Nath S, Stevens AM, Freedman BI, Tsao BP, Jacob CO, Kamen DL, Brown EE, Gilkeson GS, Alarcón GS, Reveille JD, Anaya J-M, James JA, Moser KL, Criswell LA, Vilá LM, Alarcón-Riquelme ME, Petri M, Scofield RH, Kimberly RP, Ramsey-Goldman R, Binjoo Y, Choi J, Bae S-C, Boackle SA, Vyse TJ, Guthridge JM, Namjou B, Gaffney PM, Langefeld CD, Kaufman KM, Kelly JA, Harley ITW, Harley JB, Kottyan LC. Lupus risk variants in the PXK locus alter B-cell receptor internalization. Frontiers in Genetics. 2015 Jan 8;5:450.

Kottyan LC, Weirauch MT, Rothenberg ME. Making it Big in Allergy. J Allergy Clin Immunol. 2015 Jan;135(1):43-5.

Makashir SB, Kottyan LC, Weirauch MT. Meta-analysis of Differential Gene Co-expression: Application to Lupus. Pacific Symposium on Biocomputing Proceedings. 2015.

Brungs L, Lele A, Kottyan L, Levy B, Moncrieffe H. Genetic Basis of Rheumatic Diseases and the Importance of GWAS in Paediatric Rheumatology. Annals of Pediatric Rheumatology. 2015;3(3):105-115.

Verma SS, de Andrade M, Tromp G, Kuivaniemi H, Pugh E, Namjou-Khales B, Mukherjee S, Jarvik GP, Kottyan LC, Burt A, Bradford Y, Armstrong GD, Derr K, Crawford DC, Haines JL, Li R, Crosslin D, Ritchie MD. Imputation and quality control steps for combining multiple genome-wide datasets. Frontiers in Genetics. 2014 Dec 11;5:370.

Kottyan LC, Zoller EE, Bene J, Lu X, Kelly JA, Rupert AM, Lessard CJ, Vaughn SE, Marion M, Weirauch MT, Namjou B, Adler A, Rasmussen A, Glenn S, Montgomery CG, Hirschfield GM, Xie G, Coltescu C, Amos C, Li H, Ice JA, Nath SK, Mariette X; Simon Bowman for UK primary Sjögren's syndrome registry, Rischmueller M, Lester S, Brun JG, Gøransson LG, Harboe E, Omdal R, Cunninghame-Graham DS, Vyse T, Miceli-Richard C, Brennan MT, Lessard JA, Wahren-Herlenius M, Kvarnström M, Illei GG, Witte T, Jonsson R, Eriksson P, Nordmark G; Wan-Fai Ng for UK primary Sjögren's syndrome registry, Anaya JM, Rhodus NL, Segal BM, Merrill JT, James JA, Guthridge JM, Scofield RH, Alarcon-Riquelme M, Bae SC, Boackle SA, Criswell LA, Gilkeson G, Kamen DL, Jacob CO, Kimberly R, Brown E, Edberg J, Alarcón GS, Reveille JD, Vilá LM, Petri M, Ramsey-Goldman R, Freedman BI, Niewold T, Stevens AM, Tsao BP, Ying J, Mayes MD, Gorlova OY, Wakeland W, Radstake T, Martin E, Martin J, Siminovitch K, Moser Sivils KL, Gaffney PM, Langefeld CD, Harley JB, Kaufman KM. The IRF5-TNPO3 association with systemic lupus erythematosus (SLE) has two components that other autoimmune disorders variably share. Hum Mol Genet. 2014 Jan 15;24(2):582-98.

Namjou B, Ni Y, Harley IT, Chepelev I, Cobb B, Kottyan LC, Gaffney PM, Guthridge JM, Kaufman K, Harley JB. The effect of inversion at 8p23 on BLK association with lupus in Caucasian population. PLoS One. 2014 Dec 29;9(12):e115614.

Alexander ES, Martin LJ, Collins MH, Kottyan LC, Sucharew H, He H, Mukkada VA, Succop PA, Abonia JP, Foote H, Eby MD, Grotjan TM, Greenler AJ, Dellon ES, Demain JG, Furuta GT, Gurian LE, Harley JB, Hopp RJ, Kagalwalla A, Kaul A, Nadeau KC, Noel RJ, Putnam PE, von Tiehl KF, Rothenberg ME. Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis. J Allergy Clin Immunol. 2014 Nov;134(5):1084-1092.

Fardo DW, Zhang X, Ding L, He H, Kurowski B, Alexander ES, Baye TM, Pilipenko V, Kottyan L, Nandakumar K, Martin LJ. On Family-based Genome-wide Association Studies with Large Pedigrees: Observations and Recommendations. BMC Proceedings. 2014;8(1):s26-s26.

A photo of Ashish Kumar.

Ashish R. Kumar, MD, PhD Director, Langerhans Cell Histiocytosis Center

Ashish R. Kumar, MD, PhD, is a pediatric hematologist/oncologist whose lab is investigating the biology childhood cancers and blood diseases. The current focus of research in the lab is on infant leukemia and LCH.
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513-636-7287 ashish.kumar@cchmc.org

A photo of Ashish Kumar.

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Ashish R. Kumar, MD, PhD

Director, Langerhans Cell Histiocytosis Center

Director, Hematology/Oncology Fellowship Program

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-7287

Fax 513-803-1969

Email ashish.kumar@cchmc.org

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Clinical & Research Interests

Clinical

Childhood cancer and blood disorders; immune deficiency

Research

Leukemia biology; cancer biology

Visit the Kumar Lab.

Dr. Kumar received his medical degree from L.T.M. Medical College, Mumbai, India, his PhD in anatomy and cell biology from the University of Iowa, pediatric residency training at the Mayo Clinic and fellowship in pediatric hematology / oncology / BMT at the University of Minnesota. He was appointed to the faculty of the University of Minnesota in the Department of Pediatrics where he was a member of the programs in pediatric leukemia and global pediatrics. He is currently an associate professor of pediatrics in the Division of Bone Marrow Transplantation and Immune Deficiency at Cincinnati Children's within the University of Cincinnati College of Medicine. Dr. Kumar’s laboratory is engaged in researching the biology of infant leukemia. Discoveries made in his laboratory have significantly enhanced the current understanding of leukemia. Dr. Kumar is also active in education. He has delivered invited lectures and grand round presentations on various topics.

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Learn more about the 700 Miles to Hope Bike Ride.

Dr. Kumar has been elected by peers for inclusion in the Best Doctors in America List.

Education and Training

MD: LTM Medical College, Mumbai, India.

Residency: Mayo Clinic, Rochester, MN.

Fellowship: University of Minnesota, Minneapolis, MN.

PhD: University of Iowa, Iowa City, IA.

Certification: General Pediatrics; Pediatric Hematology/Oncology Subspecialty.

Licenses: State of Ohio; State of Minnesota.

View PubMed Publications

Role of MEIS1 in hematopoiesis and hematopoietic transformation. Principal Investigator. National Institutes of Health/National Heart, Lung, and Blood Institute. Jul 2012-Jun 2017.

Novel therapeutics of targeting mTOR pathway in T-cell leukemia. Co-investigator. National Institutes of Health/National Cancer Institute. Jul 2015-Jun 2017.

A photo of Ian Lewkowich.

Ian P. Lewkowich, PhD

Ian P. Lewkowich, PhD, investigates the factors that drive the development of severe allergic asthma, with a particular focus on the molecular mechanisms through which Th17 cytokines enhance IL-13 signaling, the regulation of the asthmatic response through the PD-1/PD-L axis and the mechanisms of the well-described maternal influence in inherited asthma risk.
Visit the Lewkowich Lab.

513-636-3999 ian.lewkowich@cchmc.org

A photo of Ian Lewkowich.

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Ian P. Lewkowich, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-3999

Email ian.lewkowich@cchmc.org

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Immunology; asthma

Visit the Lewkowich Lab.

While Th2 immune responses are central to disease pathology in allergic asthma, there is a growing understanding that the Th2 paradigm is not sufficient to explain the entire spectrum of disease severity. Indeed, there is growing belief that severe disease may be driven by a different process than mild to moderate disease.

Using a mouse model of allergic asthma in which one strain develops a phenotype characteristic of mild asthma (C3H/HeJ), and others develop a phenotype characteristic of severe disease (A/J), we have identified several novel mechanisms through which asthma severity is regulated. We have found that the development of severe allergic asthma is associated with a limited capacity of Tregs to limit pulmonary dendritic cell activity, enhanced capacity for antigen uptake by pulmonary myeloid dendritic cells, and the development of a mixed Th2/Th17 immune response. In contrast, C3H mice demonstrate increased Treg activity, preferential antigen uptake by pulmonary plasmacytoid dendritic cells, and an exclusively Th2-biased immune response. We are presently using the A/J versus C3H/HeJ mouse model of allergic asthma to tease out the mechanisms responsible the development of severe allergic asthma.

Education and Training

PhD: University of Manitoba, Winnipeg, Canada, 2004.

View PubMed Publications

Lewkowich IP, Fox JG Perkins C, Lewis L, Finkelman FD Smith DE, Bryce PJ, Kurt-Jones EA, Wang TC, Sivaprasad U, Hershey GK, Herbert DR. Trefoil factor 2 rapidly induces interleukin 33 to promote type 2 immunity during allergic asthma and hookworm infection. J Exp Med. 2012;209(3):607-22.

Lufti R, Ledford JR, Zhou P, Lewkowich IP, Page K. Dendritic Cell-Derived Tumor Necrosis Factor α Modifies Airway Epithelial Cell Responses. J Innate Immun. 2012;4(5-6):542-52.

Lewkowich IP, Lajoie S, Stoffers SL, Suzuki Y, Richgels PK, Dienger K, Sproles AA, Yagita H, Hamid Q, Wills-Karp M. PD-L2 modulates asthma severity by directly decreasing dendritic cell IL-12 production. Mucosal Immunol. 2012.

Stefater JA, Lewkowich IP, Rao S, Ajima R, Mariggi G, Wills-Karp M, Pollard J, Yamaguchi T, McMahon AP, Ferrara N, Gerhardt H, Lang RA. Microglial Wnt ligands suppress retinal angiogenesis via activation of the VEGF inhibitor Flt1. Nature. 2011;474(7352):511-515.

Lewkowich IP, Day SB, Ledford JR, Zhou P, Dienger K, Wills-Karp M, Page K. Protease-activated receptor 2 activation of myeloid dendritic cells regulates allergic airway inflammation. Respir Res. 2011;(12):122.

Lewkowich IP1, Lajoie S1, Suzuki Y, Clark JR, Sproles AA, Dienger K, Budelsky A, and Wills-Karp M, Complement-mediated regulation of the IL-17A axis is a central genetic determinant of the severity of experimental allergic asthma. Nat Immunol. 2010;(10):928-935.

Chen G, Wan H, Luo F, Zhang L, Xu Y, Lewkowich IP, Wills-Karp M and Whitsett JA. Foxa2 programs Th2 cell-mediated innate immunity in the developing lung. J Immunol. 2010;(184):6133-6141.

Lewkowich IP, Lajoie S, Dienger K, Herman NS, Sproles AA, and Wills-Karp M. Enhanced allergen uptake, activation, and IL-23 production by pulmonary myeloid DCs drives airway hyperresponsiveness in asthma-susceptible mice. PLoS ONE. 2008;(3):e3879.

Köhl J, Baelder R, Lewkowich IP, Pandey MK, Hawlisch H, Wang L, Best J, Herman NS, Sproles AA, Zwirner J, Whitsett JA, Gerard C, Sfyroera G, Lambris JD, and Wills-Karp M. A regulatory role for the C5a anaphylotoxin on type 2 immunity in asthma. J Clin Invest. 2006;(116):783-796.

Lewkowich IP, Herman NS, Schleifer KW, Dance MP, Chen BL, Dienger KM, Sproles AA, Shah JS, Köhl J, Belkaid Y, and Wills-Karp M. CD4+CD25+ T cells protect against experimentally induced asthma and alter pulmonary dendritic cell phenotype and function. J Exp Med. 2005;(202):1549-1561.

A photo of Andrew W. Lindsley.

Andrew W. Lindsley, MD, PhD

Andrew W. Lindsley, MD, PhD focuses on the role of sphingolipid signaling in the pathogenesis of pediatric-onset asthma, the mechanisms of humoral immune deficiency and B cell defects associated with Kabuki syndrome and abnormal non-canonical NFϰB signaling.

513-636-4589 andrew.lindsley@cchmc.org

A photo of Andrew W. Lindsley.

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Andrew W. Lindsley, MD, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-4589

Email andrew.lindsley@cchmc.org

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Clinical & Research Interests

Clinical

Kabuki syndrome; immune deficiency

Research

Asthma pathogenesis

Education and Training

PhD: Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, 2005.

MD: Indiana University School of Medicine, Indianapolis, IN, 2007.

Residency: Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2007-10.

Fellowship: Allergy & Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2010-13.

Certifications: Pediatrics 2013, Allergy & Immunology 2014.

Lindsley AW, Saal HM, Burrow TA, Hopkin RJ, Shchelochkov O, Khandelwal P, Xie C, Bleesing J, Filipovich L, Risma K, Assa’ad AH, Roehrs PA, Bernstein JA. Defects of B Cell Terminal Differentiation in Patients with Type-1 Kabuki Syndrome. J Allergy Clin Immunol. 2015.

Lindsley AW, Qian Y, Valencia CA, Shah K, Zhang K, Assa'ad A. Combined Immune Deficiency in a Patient with a Novel NFKB2 Mutation. J Clin Immunol. 2014 Nov;34(8):910-5.

Lyons JJ, Sun G1, Stone KD, Nelson C1, Wisch L, O'Brien M, Jones N, Lindsley A, Komarow HD, Bai Y, Scott LM, Cantave D, Maric I, Abonia J, Rothenberg ME, Schwartz LB, Milner JD, Wilson TM. Mendelian inheritance of elevated serum tryptase associated with atopy and connective tissue abnormalities. J Allergy Clin Immunol. 2014 May;133(5):1471-4.

Baye T, Kovacic M, Biagini-Myers J, Martin L, Lindsey M, Patterson T, He H, Ericksen M, Gupta J, Tsoras A, Lindsley A, Rothenberg M, Wills-Karp M, Eissa N, Borish L, Hershey G. Differences in Candidate Gene Association between European Ancestry and African American Asthmatic Children. PLoS One. 2011 Feb 28;6(2):e16522.

Snider P, Hinton RB, Moreno-Rodriguez RA, Wang J, Rogers R, Lindsley A, Li F, Ingram DA, Menick D, Field L, Firulli AB, Molkentin JD, Markwald R, Conway SJ. Periostin is required for maturation and extracellular matrix stabilization of noncardiomyocyte lineages of the heart. Circ Res. 2008 Apr 11;102(7):752-60.

Lindsley A, Snider P, Zhou H, Rogers R, Wang J, Olaopa M, Kruzynska-Frejtag A, Koushik SV, Lilly B, Burch JB, Firulli AB, Conway SJ. Identification and characterization of a novel Schwann and outflow tract endocardial cushion lineage-restricted periostin enhancer. Dev Biol. 2007 Jul 15;307(2):340-55.

Lindsley A, Li W, Wang J, Maeda N, Rogers R, Conway SJ. Comparison of the four mouse fasciclin-containing genes expression patterns during valvuloseptal morphogenesis. Gene Expr Patterns. 2005 Jun;5(5):593-600.

Rios H, Koushik S, Wang J, Lindsley A, Wang H, Rogers R, Chen Z, Maeda M, Kruzynska-Frejtag A, Markwald R, Feng J, Conway S. Periostin null mice exhibit dwarfism, cardiac valve anomalies, incisor enamel defects, & an early onset periodontal disease-like phenotype. Mol Cell Biol. 2005 Dec;25(24):11131-44.

A photo of Rajat Madan.

Rajat Madan, MBBS, PhD Member, Division of Gastroenterology, Hepatology and Nutrition

The Madan Lab studies the role of obesity-associated molecule leptin in controlling host neutrophil responses to Clostridium difficile, the #1 cause of nosocomial infections in the U.S. The lab uses samples (and clinical data) from patients with C. difficile and different murine models (diet-induced obese and leptin receptor mutant mice) of C. difficile infection, to understand the role of leptin signaling in disease pathogenesis and resolution.

513-558-0220 rajat.madan@uc.edu

A photo of Rajat Madan.

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Rajat Madan, MBBS, PhD

Member, Division of Gastroenterology, Hepatology and Nutrition

Member, Division of Immunobiology

Academic Affiliations

Assistant Professor, UC Department of Internal Medicine

Phone 513-558-0220

Email rajat.madan@uc.edu

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The overall research goal of our laboratory is to better understand the cellular and molecular mechanisms by which nutrition, metabolism, and immune responses to infections are fundamentally linked. Leptin is an adipose tissue-secreted cytokine that sits at the intersection of metabolism and immunity. Interestingly obesity is a state of high serum leptin levels, thus leptin by virtue of its multiple physiologic effects is likely to play an important role in directing inflammation in obese patients as well, who represent a rapidly expanding population demographic worldwide. Clostridium difficile is the #1 cause of healthcare-associated diarrhea in the U.S. In our lab, we are investigating the role of leptin receptor polymorphisms and obesity (as measured by Body Mass Index) in affecting disease susceptibility, severity and disease outcomes in patients with C. difficile infection. In parallel, we are using various leptin transgenic mice and diet-induced obese mice to interrogate the mechanism(s) by which leptin signaling impacts the immune response during C. difficile infections. Our studies (using both human clinical samples and mouse models) have the potential to augment the current treatment paradigm for C. difficile with therapies directed at the host immune response.

Education and Training

MBBS: JLN Medical College, Ajmer, India, 2001.

PhD: Immunology and Developmental Biology, University of Cincinnati, Cincinnati, 2009.

Residency: Internal Medicine, The Christ Hospital, Cincinnati, 2011.

Fellowship: Infectious Diseases, University of Virginia, Charlottesville, 2014.

Certifications: Internal Medicine, 2011; Infectious Diseases, 2014; CTropMed® Program, 2014.

View PubMed Publications

Jose S, Madan R. Neutrophil-mediated inflammation in the pathogenesis of Clostridium difficile infections. Anaerobe. 2016.

Madan R, Petri WA Jr. Role of obesity and adipose tissue-derived cytokine leptin during Clostridium difficile infection. Anaerobe. 2015 Jan 29.

Madan R, Guo X, Naylor C, Buonomo EL, Mackay D, Noor Z, Concannon P, Scully KW, Pramoonjago P, Kolling GL, Warren CA, Duggal P, Petri WA Jr. Role of leptin-mediated colonic inflammation in defense against Clostridium difficile colitis. Infect Immun. 2014 Jan;82(1):341-9.

Naylor C, Burgess S, Madan R, Buonomo E, Razzaq K, Ralston K, Petri WA Jr. Leptin receptor mutation results in defective neutrophil recruitment to the colon during Entamoeba histolytica infection. MBio. 2014 Dec 16;5(6).

Buonomo EL, Madan R, Pramoonjago P, Li L, Okusa MD, Petri WA Jr. Role of interleukin 23 signaling in Clostridium difficile colitis. J Infect Dis. 2013 Sep;208(6):917-20.

Jarrell A, Kawsky J, Johnson T, Voss S, Madan R, Weitkamp T, Wigle P. An interdisciplinary approach to determine schistosomiasis prevalence and administer praziquantel to school-age children in Tanzania. Am J Health Syst Pharm. 2013 Nov 1;70(21):1880-2.

Madan R, Jr WA. Immune responses to Clostridium difficile infection. Trends Mol Med. 2012 Nov;18(11):658-66.

Denning TL, Norris BA, Medina-Contreras O, Manicassamy S, Geem D, Madan R, Karp CL, Pulendran B. Functional specializations of intestinal dendritic cell and macrophage subsets that control Th17 and regulatory T cell responses are dependent on the T cell/APC ratio, source of mouse strain, and regional localization. J Immunol. 2011 Jul 15;187(2):733-47.

Madan R, Demircik F, Surianarayanan S, Allen JL, Divanovic S, Trompette A, Yogev N, Gu Y, Khodoun M, Hildeman D, Boespflug N, Fogolin MB, Gröbe L, Greweling M, Finkelman FD, Cardin R, Mohrs M, Müller W, Waisman A, Roers A, Karp CL. Nonredundant roles for B cell-derived IL-10 in immune counter-regulation. J Immunol. 2009 Aug 15;183(4):2312-20.

Murai M, Turovskaya O, Kim G, Madan R, Karp CL, Cheroutre H, Kronenberg M. Interleukin 10 acts on regulatory T cells to maintain expression of the transcription factor Foxp3 and suppressive function in mice with colitis. Nat Immunol. 2009 Nov;10(11):1178-84.

Role of leptin in mucosal protection during Clostridium difficile infection. Principal Investigator. NIH. Aug 2014-July 2019.

Regulation of neutrophil recruitment during Clostridium difficile infection by a single nucleotide polymorphism in leptin receptor. Principal Investigator. Department of Medicine, University of Cincinnati. Jan 2016-Dec 2016.

A photo of Punam Malik.

Punam Malik, MD Director, Cincinnati Comprehensive Sickle Cell Center

Punam Malik, MD, works to correct the gene responsible for sickle cell anemia. One of the lab’s major projects uses gene therapy to treat sickle cell disease. The lab is also interested in gene therapy for other diseases. She has developed various methods for delivering corrective genes to cells, improving methods for gene therapy in general.

513-636-1333 punam.malik@cchmc.org

A photo of Tesfaye Mersha.

Tesfaye B. Mersha, PhD

Tesfaye B. Mersha, PhD, is the principal investigator of a federally funded mentored research science award (K01). The goals of his research are to develop and evaluate an efficient approach to localize asthma liability genes in diverse African American populations in collaboration with members of the Department of Environmental Health at the University of Cincinnati, and to identify genes and regulatory networks that impact onset and severity of eczema.
Visit the Mersha Lab.

513-803-2766 tesfaye.mersha@cchmc.org

A photo of Tesfaye Mersha.

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Tesfaye B. Mersha, PhD

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-803-2766

Fax 513-636-1657

Email tesfaye.mersha@cchmc.org

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Clinical & Research Interests

Clinical

Allergy and allergy related disorders

Research

Quantitative and statistical genetics and genomics; genetic linkage, association and admixture analysis; expression analysis; network and pathway analysis; gene ontology and functional commonalities analysis

Visit Dr Mersha's external lab website.

Visit Dr. Mersha's lab at Cincinnati Children's.

Dr. Mersha is currently an associate professor at the Cincinnati Children’s Hospital Medical Center and University of Cincinnati, where he leads the Population Genetics, Ancestry, and Bioinformatics (pGAB) Laboratory. Dr. Mersha’s research combines quantitative, ancestry and statistical genomics to unravel genetic and non-genetic contributions to complex diseases and racial disparities in human populations, particularly asthma and asthma-related allergic disorders. Much of his research is at the interface of genetic ancestry, statistics, bioinformatics, and functional genomics, and he is interested in cross-line disciplines to unravel the interplay between genome and envirome underlying asthma risk. Dr. Mersha’s laboratory carries out both computational and applied data analysis projects, including the development of statistical and genome informatics tools that enable multiethnic admixture, genome-wide association and omics integration studies of complex biomedical traits, including asthma. He is a recognized expert in the field of genetic ancestry, race, admixture mapping and mining functional genomic databases related to complex diseases.

Dr. Mersha’s team contributions include the development of: 1) AncestrySNPminer, the first web-based bioinformatics tool designed to retrieve ancestry-informative markers (AIMs) with divergent allele frequency/selection pressure from the genomic databases (Cincinnati Children's Hospital Medical Center Technology disclosure #: 2011-1105). As of March 15, 2018, over 18,506 registered users world-wide have freely accessed this tool; 2) GENEASE, an integrative omics tool used to filter functionally important variants from publicly available ‘omics’ databases such as ENCODE, GTEx, and Epigenome Roadmap; 3) SAGE, a shared ancestry genetic etiology miner tool among complex diseases and multiple racial ancestry populations; 4) AdmixPower, a power and sample size estimation for mapping genetic loci in admixed populations.

Dr. Mersha has received multiple awards and honors including 1) 2017 Faculty Research Achievement Award from Cincinnati Children’s Hospital Medical Center, 2) 2017 African Professionals Network (APNET) Business & Professional Achievement Award, and 3) Keystone Symposia Early Career Investigator Award. Dr. Mersha has been invited to speak at national and international conferences, and moderated a panel on use of ancestry, race and ethnicity in biomedical research at a recent NIH conference. In 2017, he was invited to speak at the NHLBI funded PRIDE meeting on the topic of “My Road to Success.” Dr. Mersha organized and led an “Omics” workshop at the 2017 AAAAI annual conference entitled: “Omics-based bioinformatics/system biology approach to allergic disorders”. Dr. Mersha is a Program Faculty member of the Immunology Graduate Program, Biomedical Informatics (BMI) Graduate Program Faculty, Medical Scientist Training Program (MSTP) Faculty, and Systems Biology Program Faculty, and offer lectures to graduate students at the University of Cincinnati and Xavier University.

A major focus of Dr. Mersha's laboratory has been ancestry analysis, gene-environment interactions and functional genomics of asthma and asthma-related allergic disorders. Specific ongoing research projects include the following: 1) admixture mapping to localize asthma liability genes in admixed population; 2) interaction of asthma risk variants and environmental exposures that shape racial disparities; 3) identifying genetic/regulatory networks to identify potential functional variants associated with asthma and atopic dermatitis using whole transcriptome RNA-seq profiling; 4) investigating the role of microbiome and epigenome on asthma pathogenesis among immigrants; 5) developing web-based bioinformatics tools designed to leverage and integrate multiple omics from public databases (e.g., ENCODE, Epigenome Roadmap, GTEx, GEO and 1000 Genomes Project). His career goals are to develop a program that will lead to an in-depth understanding of the complex interplay between genomic variations and environmental exposure risk factors in the etiology of complex diseases, including asthma. His ultimate goal is to translate these findings into the clinic through collaborations with clinicians.

Education and Training

BS: Alemaya University, Ethiopia, 1992.

MS: Alemaya University, Ethiopia, 1996.

PhD: University of Göttingen, Germany, 2004.

View PubMed Publications

Mersha TB. Mapping asthma-associated variants in admixed populations. Front Genet. 2015 Sep 29;6:292.

Ghosh D, Ding L, Sivaprasad U, Geh E, Biagini Myers J, Bernstein JA, Khurana Hershey GK, Mersha TB. Multiple Transcriptome Data Analysis Reveals Biologically Relevant Atopic Dermatitis Signature Genes and Pathways. PLoS One. 2015 Dec 30;10(12):e0144316.

Mersha TB, Abebe T. Self-reported race/ethnicity in the age of genomic research: its potential impact on understanding health disparities. Hum Genomics. 2015 Jan 7;9:1.

Ding L, Abebe T, Beyene J, Wilke RA, Goldberg A, Woo JG, Martin LJ, Rothenberg ME, Rao M, Hershey GK, Chakraborty R, Mersha TB. Rank-based genome-wide analysis reveals the association of Ryanodine receptor-2 gene variants with childhood asthma among human populations. Hum Genomics. 2013 Jul 5;7:16.

Amirisetty S, Hershey GK, Baye TM. AncestrySNPminer: A bioinformatics tool to retrieve and develop ancestry informative SNP panels. Genomics. 2012 Jul;100(1):57-63.

Baye TM, Butsch Kovacic M, Biagini Myers JM, Martin LJ, Lindsey M, Patterson TL, He H, Ericksen MB, Gupta J, Tsoras AM, Lindsley A, Rothenberg ME, Wills-Karp M, Eissa NT, Borish L, Hershey GK. Differences in Candidate Gene Association between European Ancestry and African American Asthmatic Children. PLoS One. 2011 Feb 28;6(2):e16522.

Baye TM, Abebe T, Wilke RA. Genotype-environment interaction and its translational implications. Personalized Medicine. 2011;8:59-70.

Baye TM, Wilke RA. Mapping genes that predict treatment outcome in admixed populations. Pharmacogenomics J. 2010 Dec;10(6):465-77.

Baye TM, Martin LJ, Khurana Hershey GK. Application of genetic/genomic approaches to allergic disorders. J Allergy Clin Immunol. 2010 Sep;126(3):425-36; quiz 437-8.

Baye TM, Wilke RA, Olivier M. Genomic and geographic distribution of private SNPs and pathways in human populations. Per Med. 2009 Nov 1;6(6):623-641.

A photo of Alexander Miethke.

Alexander G. Miethke, MD Medical Director, Liver Transplant Program

Alexander G. Miethke, MD, is interested in susceptibility factors for neonatal liver injury, including biliary atresia. He focuses on the interaction between the maturing adaptive immune system and hepatic immune responses to infectious insults during the early neonatal period.
Visit the Center for Autoimmune Liver Disease.

513-636-8948 alexander.miethke@cchmc.org

A photo of Alexander Miethke.

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Alexander G. Miethke, MD

Medical Director, Liver Transplant Program

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-8948

Email alexander.miethke@cchmc.org

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Clinical & Research Interests

Clinical

Pediatric liver disease including biliary atresia, inherited liver diseases, autoimmune hepatitis, and primary sclerosing cholangitis; gastrointestinal problems in children with bone marrow failure syndromes

Research

Immune mediated liver injury, specifically the role of regulatory T cells in biliary atresia and primary sclerosing cholangitis; genetic basis for intrahepatic cholestasis in children; acute liver failure in infants with mitochondrial disorders

Alexander G. Miethke, MD, joined the Division of Gastroenterology, Hepatology and Nutrition as a fellow in 2005, after completing his Pediatric Residency Training at Cincinnati Children's Hospital Medical Center. Following the completion of his fellowship, he pursued an additional year of training in pediatric transplant hepatology under the mentorship of Dr. William Balistreri and the physicians and surgeons of the Pediatric Liver Care Center.

In 2009, Dr. Miethke was appointed assistant professor of pediatrics in the Division of Gastroenterology, Hepatology and Nutrition and the Pediatric Liver Care Center at Cincinnati Children's within the UC Department of Pediatrics. His basic science research interests include the role of regulatory T cells in biliary atresia and other immune mediated liver diseases and the genetic basis of chronic cholestasis syndromes.

Education and Training

MD: Humboldt-University, Berlin, Germany, 2000.

Residency: Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2002-2004.

Fellowship: Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2005-2007.

Advanced Fellowship: Pediatric Transplant Hepatology, University of Cincinnati and Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2009.

Certification: Pediatrics, 2005; Pediatric Gastroenterology, 2009; Pediatric Transplant Hepatology, 2010.

View PubMed Publications

Evason K, Bove KE, Finegold MJ, Knisely AS, Rhee S, Rosenthal P, Miethke AG, Karpen SJ, Ferrell LD, Kim GE. Morphologic findings in progressive familial intrahepatic cholestasis 2 (PFIC2): correlation with genetic and immunohistochemical studies. Am J Surg Pathol. 2011;35:687-96.

Miethke AG, Saxena V, Shivakumar P, Sabla GE, Simmons J, Chougnet CA. Post-natal paucity of regulatory T cells and control of NK cell activation in experimental biliary atresia. J Hepatol. 2010 May;52(5):718-26.

Liu C, Aronow BJ, Jegga AG, Wang N, Miethke A, Mourya R, Bezerra JA. Novel resequencing chip customized to diagnose mutations in patients with inherited syndromes of intrahepatic cholestasis. Gastroenterology. 2007 Jan;132(1):119-26.

Shivakumar P, Campbell KM, Sabla GE, Miethke A, Tiao G, McNeal MM, Ward RL, Bezerra JA. Obstruction of extrahepatic bile ducts by lymphocytes is regulated by IFN-gamma in experimental biliary atresia. J Clin Invest. 2004 Aug;114(3):322-9.

A photo of Emily Miraldi.

Emily R. Miraldi, PhD

Dr. Miraldi is a computational and systems biologist who builds mathematical models of the immune system from high-dimensional genomics measurements. Her studies leverage biotechnologies, including chromatin accessibility and single-cell gene expression measurements, and require new computational methods development. Miraldi’s long-term goal is to use these models to reengineer immune-cell behavior in the context of autoimmune and other diseases.
Visit the Miraldi Lab.

513-517-2063 emily.miraldi@cchmc.org

A photo of Emily Miraldi.

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Emily R. Miraldi, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-517-2063

Email emily.miraldi@cchmc.org

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Research Interests

Systems biology; computational immunology; immuno-engineering; network inference

Our research goal is immuno-engineering: to alter the behavior of specific immune cell populations in disease contexts (autoimmune disease, organ transplant, and cancer) without compromising the body’s homeostatic immune function (e.g. defense against pathogens). Thus, it is critical to develop a nuanced understanding of how different immune cells sense and respond to environmental cues across the body, in both physiological and disease settings. To this end, our lab’s major focus is reverse-engineering the underlying logic of immune cells (molecular networks that drive cellular responses) from high-dimensional molecular measurements of immune cells in action (sensing and responding to perturbations, disease conditions, etc.).

The lab’s focus is transcriptional regulatory network inference, modeling gene expression as a function of transcription factor activities, from gene expression and measurements of chromatin state. Chromatin accessibility measurements by ATAC-seq, together with transcription-factor DNA-binding preferences (motifs), can be used to broadly profile potential transcription factor binding events in relatively small populations of cells. Thus, we have used ATAC-seq with RNA-seq to enable de novo inference of transcriptional regulatory networks in physiological settings where sample material is limiting (e.g., intestinal immune cells in response to microbial/genetic perturbations). To date, most of these efforts have been in mouse models, as it is generally not possible to obtain sufficient sample material for similar experimental designs in human. To build human immune cell models, we are developing multi-task learning approaches to leverage evolutionarily conserved relationships and borrow statistical power from mouse datasets for inference in human. We are also developing methods to enable transcriptional regulatory network inference in very rare cell populations, as measured from single-cell RNA-seq experiments.

Learn more about the Miraldi Lab.

Education and Training

BA: Oberlin College, Oberlin, OH.

PhD: Massachusetts Institute of Technology, Cambridge, MA.

Postdoctoral Fellow: New York University, New York School of Medicine, Flatiron Institute (Simons Foundation), New York, NY.

View PubMed Publications

Karwacz K, Miraldi ER, Pokrovskii M, Madi A, Yosef N, Wortman I, Chen X, Watters A, Carriero N, Awasthi A, Regev A, Bonneau R, Littman DR, Kuchroo VK. Critical role of IRF1 and BATF in preparing the chromatin landscape during Tr1 differentiation. Nature Immunology. 2017.

Rocha PP, Raviram R, Fu Y, Kim J, Luo V, Aljoufi A, Swanzey E, Pasquarella A, Balestrini A, Miraldi ER, Bonneau R, Petrini J, Schotta G, Skok JA. A damage-independent role for 53BP1 that impacts break order and Igh architecture during class switch recombination. Cell Rep. 2016 Jun 28;16(1):48-55.

Raviram R, Rocha PD, Mueller CL, Miraldi ER, Fu Y, Swanzey E, Badri S, Proudhon C, Snetkova V, Bonneau R, Skok JA. 4C-ker: A method to reproducibly identify genome-wide interactions captured by 4C-Seq experiments. PLoS Comput Biol. 2016 Mar 3;12(3):e1004780.

Huang W, Thomas B, Flynn RA, Gavzy SJ, Wu L, Kim SV, Hall JA, Miraldi ER, Ng CP, Lee B, Rigo FW, Meadows S, Montoya NR, Herrera N, Domingos AI, Rastinejad F, Myers RM, Fuller-Pace FV, Bonneau R, Chang HY, Acuto O, Littman DR. DDX5 and its associated lncRNA Rmrp modulate Th17 cell effector functions. Nature. 2015 Dec 24;528(7583):517-22.

Sano T, Huang W, Hall JA, Chen A, Gravzy SJ, Lee J, Ziel J, Miraldi ER, Domingos AJ, Bonneau R, Littman DR. An IL-23R/IL-22 circuit regulates epithelial serum amyloid A to promote local effector Th17 responses. Cell. 2015;163(2):381-393.

Kurtz ZD, Mueller CL, Miraldi ER, Littman DR, Blaser MJ, Bonneau R. Sparse and compositionally robust inference of microbial ecological networks. PLoS Computational Biology. 2015;11(5):e1004226.

Yu B, Doraiswamy H, Chen X, Miraldi ER, Ortiz M, Hafemeister C, Bonneau R, Silva CT. Genotet: an interactive web-based visual exploration framework to support validation of gene regulatory networks. IEEE Trans Vis Comput Graph. 2014 Dec;20(12):1903-12.

Longman RS, Diehl GE, Victorio DA, Huh JH, Galan C, Miraldi ER, Swaminath A, Bonneau R, Scherl EJ, Littman DR. CX3CR1+ mononuclear phagocytes support colitis-associated innate lymphoid cell production of IL-22. Journal of Experimental Medicine. 2014;211(8):1571-1583.

Miraldi ER, Sharfi H, Friedline RH, Johnson H, Zhang T, Lau K, Ko HJ, Curran TG, Haigis KM, Yaffe YB, Bonneau R, Lauffenburger DA, Kahn BB, Kim J, Neel BG, Saghatelian A, White FM. Molecular network analysis of protein-tyrosine phosphorylation and altered lipid metabolism in liver-specific PTP1b deletion mice. Integrative Biology. 2013;5(7):940-963.

Huang PH, Miraldi ER, Xu AM, Kundukulam VA, Del Rosario AM, Flynn RA, Cavenee WK, Furnari FB, White FM. Phosphotyrosine signaling analysis of site-specific mutations on EGFRvIII identifies determinants governing glioblastoma cell growth. Molecular BioSystems. 2010;6(7):1227-37.

Miraldi ER, Thomas PJ, Romberg L. Allosteric models for cooperative polymerization of linear polymers. Biophysical Journal. 2008;95(5):2470-2486.

A photo of Ardythe L. Morrow.

Ardythe L. Morrow, PhD Director, Center for Interdisciplinary Research in Human Milk and Lactation

513-636-7584 ardythe.morrow@cchmc.org

A photo of Ardythe L. Morrow.

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Ardythe L. Morrow, PhD

Director, Center for Interdisciplinary Research in Human Milk and Lactation

Global Health Center

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-7584

Fax 513-636-7509

Email ardythe.morrow@cchmc.org

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Clinical Interests

Human milk; child health and nutrition

Dr. Morrow received her MSc in nutrition from the University of the West Indies, Kingston, Jamaica (1980) and PhD in epidemiology from the University of Texas at Houston (1991). Since 1987 she has worked with colleagues in Mexico, Boston, and Houston on an NIH-funded program project on human milk immune protection against infectious disease.

She is currently professor of pediatrics at Cincinnati Children's Hospital Medical Center within the University of Cincinnati College of Medicine. She founded and directs the Center for Epidemiology and Biostatistics that has 35 faculty and staff and a multi-disciplinary Human Milk Research Program that includes clinical and basic science investigators in eight divisions.

She has published extensively on breastfeeding promotion and human milk protection against infectious diseases. Her primary focus is on protection by human milk glycans and protection against infectious disease, but she has expanded her research to understanding the relationship between breastfeeding and chronic diseases. She has been an ad hoc reviewer for NIH on breastfeeding research and a technical advisor for international breastfeeding policy and programs for Gates Foundation, UNICEF, and WHO, is on the editorial board of the Journal of Human Lactation and the journal of the Academy of Breastfeeding Medicine. She is an elected member of the American Pediatric Society. She has over 100 publications, and is the primary author of the WHO monograph, Community-based Strategies for Breastfeeding Promotion and Support in Developing Countries (2004).

She has served as chair of the Milk Club of the (American) Society for Pediatric Research for the past four years. In 1997, she received a Young Investigator award from ISRHML for her randomized trial of breastfeeding support (Lancet, 1999). She was co-organizer of the 2002 ISRHML international meeting in Mexico and is co-editor of the book "Protecting Infants through Human Milk: Advancing the Scientific Evidence."

Education and Training

BA: Rice University, Houston, TX.

MSc: University of the West Indies, Kingston, Jamaica.

PhD: The University of Texas School of Public Health, Houston, TX, 1991.

View PubMed Publications

South AP, Wessel JJ, Sberna A, Patel M, Morrow AL. Hospital readmission among infants with gastroschisis. J Perinatol. 2011 Feb 10.

Morrow AL, Meinzen-Derr J, Huang P, Schibler KR, Cahill T, Keddache M, Kallapur SG, Newburg DS, Tabangin M, Warner BB, Jiang X. Fucosyltransferase 2 Non-Secretor and Low Secretor Status Predicts Severe Outcomes in Premature Infants. J Pediatr. 2011 May;158(5):745-51.

Farkas T, Cross RW, Hargitt E 3rd, Lerche NW, Morrow AL, Sestak K. Genetic diversity and histo-blood group antigen interactions of rhesus enteric caliciviruses. J Virol. 2010 Sep;84(17):8617-25.

Woo JG, Guerrero ML, Altaye M, Ruiz-Palacios GM, Martin LJ, Dubert-Ferrandon A, Newburg DS, Morrow AL. Human milk adiponectin is associated with infant growth in two independent cohorts. Breastfeed Med. 2009 Jun;4(2):101-9.

Huang P, Morrow AL, Jiang X. The carbohydrate moiety and high molecular weight carrier of histo-blood group antigens are both required for norovirus-receptor recognition. Glycoconj J. 2009 Nov;26(8):1085-96.

Meinzen-Derr J, Morrow AL, Hornung RW, Donovan EF, Dietrich KN, Succop PA. Epidemiology of necrotizing enterocolitis temporal clustering in two neonatology practices. J Pediatr. 2009 May;154(5):656-61.

Geraghty SR, Khoury JC, Morrow AL, Lanphear BP. Reporting individual test results of environmental chemicals in breast milk: potential for premature weaning. Breastfeed Med. 2008 Dec;3(4):207-13.

Olsen IE, Lawson ML, Meinzen-Derr J, Sapsford AL, Schibler KR, Donovan EF, Morrow AL. Use of a body proportionality index for growth assessment of preterm infants. J Pediatr. 2009 Apr;154(4):486-91.

Meinzen-Derr J, Poindexter B, Wrage L, Morrow AL, Stoll B, Donovan EF. Role of human milk in extremely low birth weight infants' risk of necrotizing enterocolitis or death. J Perinatol. 2009 Jan;29(1):57-62.

Woo JG, Dolan LM, Morrow AL, Geraghty SR, Goodman E. Breastfeeding helps explain racial and socioeconomic status disparities in adolescent adiposity. Pediatrics. 2008 Mar;121(3):e458-65.

A photo of Takahisa Nakamura.

Takahisa Nakamura, PhD

Takahisa Nakamura, PhD, research goal is to address questions concerning why and how inflammatory responses are initiated, coordinated, and thus involved in the development of obesity-induced metabolic diseases.

Visit the Nakamura Lab.

513-636-4744 takahisa.nakamura@cchmc.org

A photo of Takahisa Nakamura.

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Takahisa Nakamura, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-4744

Email takahisa.nakamura@cchmc.org

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RNA-related inflammation in obesity and metabolic diseases

Visit the Nakamura Lab.

Dr. Nakamura received his PhD from the University of Tokyo in 2003. He completed postdoctoral training in the laboratory of Dr. Gökhan S. Hotamisligil at Harvard School of Public Health in 2013, followed by his faculty appointment at Cincinnati Children's Hospital Medical Center within the UC Department of Pediatrics in 2013.

Education and Training

PhD: University of Tokyo, 2003.

Postdoctoral Fellow: University of Tokyo, 2003-2006.

Research Fellow: Harvard University, 2006-2010.

Research Associate: Harvard University, 2010-2013.

View PubMed Publications

Nakamura T, Arduini A, Baccaro B, Furuhashi M, Hotamisligil GS. Small molecule inhibitors of PKR improve glucose homeostasis in obese, diabetic mice. Diabetes. 2014 Feb;63(2):526-34.

Lu B, Nakamura T, Inouye K, Li J, Tang Y, Lundbäck P, Valdes-Ferrer SI, Olofsson PS, Kalb T, Roth J, Zou Y, Erlandsson-Harris H, Yang H, Ting JP, Wang H, Andersson U, Antoine DJ, Chavan SS, Hotamisligil GS, Tracey KJ. Novel role of PKR in inflammasome activation and HMGB1 release. Nature. 2012 Aug 20;488(7413):670-4.

Morita M. Oike Y, Nagashima T, Kadomatsu T, Tabata M, Suzuki T, Nakamura T, Yoshida N, Okada M, Yamamoto T. Obesity resistance and increased hepatic expression of catabolism-related mRNAs in Cnot3(+/-) mice. EMBO J. 2011 Sep 6;30(22):4678-4691.

Nakamura T, Furuhashi M, Li P, Cao H, Tuncman G, Sonenberg N, Gorgun CZ, Hotamisligil GS. Double-stranded RNA-dependent Protein Kinase Links Pathogen Sensing with Stress and Metabolic Homeostasis. Cell. 2010 Feb 5;140(3):338-48.

Yoneda M, Suzuki T, Nakamura T, Ajima R, Yoshida Y, Kakuta S, Sudo K, Iwakura Y, Shibutani M, Mitsumori K, Yokota J, Yamamoto T. Deficiency of antiproliferative family protein Ana correlates with development of lung adenocarcinoma. Cancer Sci. 2009 Feb;100(2):224-232.

Ajima R, Akiyama T, Usui M, Yoneda M, Yoshida Y, Nakamura T, Minowa O, Noda M, Tanaka S, Noda T, Yamamoto T. Osteoporotic bone formation in mice lacking tob2; involvement of Tob2 in RANK ligand expression and osteoclasts differentiation. FEBS Lett. 2008 Apr 16;582(9):1313-8.

Morita M, Suzuki T, Nakamura T, Yokoyama K, Miyasaka T, Yamamoto T. Depletion of mammalian CCR4b deadenylase triggers elevation of the p27Kip1 mRNA level and impairs cell growth. Mol Cell Biol. 2007 Jul;27(13):4980-90.

Nakamura T, Yao R, Ogawa T, Suzuki T, Ito C, Tsunekawa N, Inoue K, Ajima R, Miyasaka T, Yoshida Y, Ogura A, Toshimori K, Noce T, Yamamoto T, Noda T. Oligoasthenoteratozoospermia in mice lacking Cnot7, a regulator of retinoid X receptor beta. Nat Genet. 2004 May;36(5):528-33.

Kimura H*, Nakamura T*, Ogawa T, Tanaka S, Shiota K. Transcription of mouse DNA methyltransferase 1 (Dnmt1) is regulated by both E2F-Rb-HDAC-dependent and -independent pathways. Nucleic Acids Res. 2003 Jun 15;31(12):3101-13. *These authors contributed equally to this work.

Yoshida Y*, Nakamura T*, Komoda M, Satoh H, Suzuki T, Tsuzuku JK, Miyasaka T, Yoshida EH, Umemori H, Kunisaki RK, Tani K, Ishii S, Mori S, Suganuma M, Noda T, Yamamoto T. Mice lacking a transcriptional corepressor Tob are predisposed to cancer. Genes Dev. 2003 May 15;17(10):1201-6. *These authors contributed equally to this work.

Analysis of pathogenic double-stranded RNA in chronic inflammatory diseases. Principal Investigator. Japan Science and Technology Agency, PRESTO. Feb 2013–Mar 2016.

A photo of Chandrashekhar Pasare.

Chandrashekhar Pasare, DVM, PhD

Chandrashekhar Pasare, DVM, PhD, investigates the mechanisms by which the innate immune system regulates adaptive immune responses. He is also interested in role of Toll-like receptors in innate immunity and inflammation. The overall goal of his research is to provide molecular and cellular insights into how the activation of pattern recognition receptors in cells of the innate immune system induces tailored adaptive immune responses necessary for elimination of specific pathogens.

513-636-6656 chandrashekhar.pasare@cchmc.org

A photo of Chandrashekhar Pasare.

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Chandrashekhar Pasare, DVM, PhD

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-6656

Email chandrashekhar.pasare@cchmc.org

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Research Interests

Innate immunity; toll-like receptor signaling; dendritic cell biology; innate control of adaptive immunity; regulation of inflammation

Dr. Pasare's laboratory is involved in studying the Toll-like receptor signaling pathway in cells of the innate immune system and also investigating the mechanisms by which these receptors regulate adaptive immune responses. Toll-like receptors are a major family of pattern recognition receptors of the innate immune systems and sense presence of bacterial, fungal and viral pathogens. Activation of these receptors leads to secretion of cytokines and chemokine that are important for protection against pathogens. However unregulated production of cytokines and chemokine leads to inflammation associated with both auto-inflammatory and auto-immune diseases. Work in the Pasare lab has led to novel insights into several aspects of both innate and adaptive immunity. His lab identified BCAP to be a novel adapter of the TLR signaling pathway and its importance in linking TLR signaling to PI3 Kinase activation and dampening of inflammatory responses. Work from his laboratory also led to discovery of a rapid NLRP3 inflammasome activation pathway this is specifically regulated by IRAK1. Work in his laboratory led to also identified a crucial role for IL-1R signaling in regulating effector function of CD4 T cells of all lineages. His current focus is to gain molecular understanding of inflammation and to tease out the complex cross-talk between innate and adaptive immune systems.

Education and Training

PhD: National Institute of Immunology, New Delhi, India, 2000.

Post Doctoral Fellowship: Immunobiology, Yale University School of Medicine, New Haven, CT, 2006.

View PubMed Publications

Deason K, Troutman TD, Jain A, Challa DK, Mandraju R, Brewer T, Ward ES, Pasare C. BCAP links IL-1R to the PI3K-mTOR pathway and regulates pathogenic Th17 cell differentiation. J Exp Med. 2018 Aug 9.

Jain A, Song R, Wakeland EK, Pasare C. T cell-intrinsic IL-1R signaling licenses effector cytokine production by memory CD4 T cells. Nat Commun. 2018 Aug 9;9(1):3185.

Mandraju R, Jain A, Gao Y, Ouyang Z, Norgard MV, Pasare C. MyD88 Signaling in T Cells Is Critical for Effector CD4 T Cell Differentiation following a Transitional T Follicular Helper Cell Stage. Infect Immun. 2018 Apr 23;86(5).

Jain A, Pasare C. Innate Control of Adaptive Immunity: Beyond the Three-Signal Paradigm. J Immunol. 2017 May 15;198(10):3791-3800.

Akbar MA, Mandraju R, Tracy C, Hu W, Pasare C, Krämer H. ARC Syndrome-Linked Vps33B Protein Is Required for Inflammatory Endosomal Maturation and Signal Termination. Immunity. 2016 Aug 16;45(2):267-79.

Hu W, Jain A, Gao Y, Dozmorov IM, Mandraju R, Wakeland EK, Pasare C. Differential outcome of TRIF-mediated signaling in TLR4 and TLR3 induced DC maturation. Proc Natl Acad Sci U S A. 2015 Nov 10;112(45):13994-9

Mandraju R, Murray S, Forman J, Pasare C. Differential ability of surface and endosomal TLRs to induce CD8 T cell responses in vivo. J Immunol. 2014 May 1;192(9):4303-15.

Lin KM, Hu W, Troutman TD, Jennings M, Brewer T, Li X, Nanda S, Cohen P, Thomas JA, Pasare C. IRAK-1 bypasses priming and directly links TLRs to rapid NLRP3 inflammasome activation.
Proc Natl Acad Sci U S A. 2014 Jan 14;111(2):775-80.

Troutman TD, Hu W, Fulenchek S, Yamazaki T, Kurosaki T, Bazan JF, Pasare C. Role for B-cell adapter for PI3K (BCAP) as a signaling adapter linking Toll-like receptors (TLRs) to serine/threonine kinases PI3K/Akt. Proc Natl Acad Sci U S A. 2012 Jan 3;109(1):273-8.

Hu W, Troutman TD, Edukulla R, Pasare C. Priming microenvironments dictate cytokine requirements for T helper 17 cell lineage commitment. Immunity. 2011 Dec 23;35(6):1010-22.

Innate mechanisms of regulation of Th17 responses. Principal Investigator. National Institutes of Health/NIAID. Dec 2016-Nov 2021.

Role of BCAP in regulating inflammation and adaptive immunity. Principal Investigator. National Institutes of Health/National Institute of Allergy and Infectious Diseases. Aug 2015-Jan 2020.

Endocytic Trafficking and Cell Signaling in Models of ARC Syndrome. Co-Investigator. National Institutes of Health/National Institute of General Medical Sciences. Apr 2017-Mar 2021.

A photo of Joseph Qualls.

Joseph E. Qualls, PhD

Joseph E. Qualls, PhD, examines the cellular and molecular facets of macrophage biology during health and disease. This white blood cell has an unprecedented role in regulating inflammation, pathogen elimination and maintaining tissue homeostasis. Specifically, Dr. Qualls’ laboratory focuses on amino acid utilization by macrophages, and how this affects the outcome of infection and inflammatory disease.

513-636-9102 joseph.qualls@cchmc.org

A photo of Joseph Qualls.

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Joseph E. Qualls, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-636-9102

Email joseph.qualls@cchmc.org

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Immunology; innate immunity; macrophage biology; amino acid metabolism; intracellular pathogenesis

Visit the Qualls Lab.

Dr. Qualls completed his undergraduate work in 2002, receiving his BA summa cum laude in biology from Thomas More College in Crestview Hills, KY. He then joined the laboratory of Don Cohen, PhD, in the Department of Microbiology, Immunology, and Molecular Genetics at the University of Kentucky, where he studied the role of macrophages and dendritic cells during the development of inflammatory bowel disease. After defending his thesis and receiving his PhD in 2007, Dr. Qualls began his postdoctoral training with Peter Murray, PhD, in the Department of Infectious Diseases and Immunology at St. Jude Children’s Research Hospital in Memphis, TN, where his research helped to define the functional plasticity of macrophages in response to infection and cancer. During his postdoctoral training, Dr. Qualls received a Ruth L. Kirschstein National Research Service Award and actively participated as vice chair of mentoring activities within the Postdoctoral Association Council and as a member of the Education Programs Committee.

Dr. Qualls’ long-term goals are to understand the interplay between nutrition, metabolism, and immune regulation during anti-pathogen defense. He has focused on how macrophages use the amino acid, L-arginine, to combat intracellular pathogens. As a starting point to appreciate broader principles of immunity and metabolism he established a map of L-arginine metabolism at the transcriptomic and metabolomic levels. His laboratory now uses this map to dissect how L-arginine generates anti-microbial effectors, how this pathway is regulated, and how microbes can hijack the pathway. His current research has two complementary tracks that retain initial focus on L-arginine metabolism in macrophages, but will eventually broaden into larger issues concerning metabolism in immunity.

The Qualls laboratory is currently addressing the provocative role of L-arginine biosynthesis from L-citrulline during intracellular infection, how this mechanism is regulated at the cellular level (predominantly in macrophages and T cells), and the mechanism(s) of L-arginine/L-citrulline-mediated immune cell function. While greatly unexplored, this pathway of amino acid recycling and utilization is vital as mice deficient in L-arginine biosynthesis, compared to normal mice, lack efficient control of M. tuberculosis infection.

Education and Training

BA: Thomas More College, Crestview Hills, KY, 2002.

PhD: University of Kentucky, Lexington, KY, 2007.

Postdoctoral Fellowship: St. Jude Children’s Research Hospital, Memphis, TN, 2012.

View PubMed Publications

Lange SM, McKell MC, Schmidt SM, Hossfeld AP, Chaturvedi V, Kinder JM, McAlees JW, Lewkowich IP, Way SS, Turner J, Qualls JE. L-Citrulline Metabolism in Mice Augments CD4(+) T Cell Proliferation and Cytokine Production In Vitro, and Accumulation in the Mycobacteria-Infected Lung. Front Immunol. 2017 Nov 16;8:1561.

Marigo I, Zilio S, Desantis G, Mlecnik B, Agnellini AH, Ugel S, Sasso MS, Qualls JE, Kratochvill F, Zanovello P, Molon B, Ries CH, Runza V, Hoves S, Bilocq AM, Bindea G, Mazza EM, Bicciato S, Galon J, Murray PJ, Bronte V. T Cell Cancer Therapy Requires CD40-CD40L Activation of Tumor Necrosis Factor and Inducible Nitric-Oxide-Synthase-Producing Dendritic Cells. Cancer Cell. 2016 Sep 12;30(3):377-90.

Rapovy SM, Zhao J, Bricker RL, Schmidt SM, Setchell KDR, Qualls JE. Differential requirements for L-citrulline and L-arginine during anti-mycobacterial macrophage activity. Journal of Immunology. 2015 Oct 1;195(7):3293-300.

Kratochvill F, Neale G, Haverkamp JM, Van de Velde L, Smith AM, Kawauchi D, McEvoy J, Roussel MF, Dyer MA, Qualls JE, Murray PJ. TNF counterbalances the emergence of M2 tumor macrophages. Cell Reports. 2015 Sep 22;12(11):1902-14.

Haverkamp JM, Smith AM, Weinlich R, Dillon CP, Qualls JE, Neale G, Koss B, Kim Y, Bronte V, Herold MJ, Green DR, Opferman JT, Murray PJ. Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways. Immunity. 2014 Dec 18;41(6):947-59.

Duque-Correa MA, Kuhl A, Rodriquez PC, Zedler U, Schommer-Leitner S, Rao M, Weiner J, Hurwitz R, Qualls JE, Kosmiadi GA, Murray PJ, Kaufmann SHE, Reece ST. Macrophage arginase-1 controls bacterial growth and pathology in hypoxic tuberculosis granulomas. Proceedings of the National Academy of Sciences – USA. 2014 Sep 23;111(38):E4024-32.

Qualls JE, Subramanian C, Smith AM, Balouzian L, DeFreitas AA, Shirey KA, Reutterer B, Kernbauer E, Stockinger S, Decker T, Miyairi I, Vogel SN, Rock CO, Murray PJ. Sustained generation of nitric oxide and control of mycobacterial infection requires argininosuccinate synthase 1. Cell Host & Microbe. 2012 Sep 13;12(3):313-23.

Smith AM, Qualls JE, O’Brien K, Balouzian L, Johnson PF, Schultz-Cherry S, Smale ST, Murray PJ. A Distal Enhancer in Il12b is the Target of Transcriptional Repression by the Stat3 Pathway and Requires the B-Zip Protein NFIL-3. Journal of Biological Chemistry. 2011 Jul 1; 286(26):23582-90.

Qualls JE, Neale G, Smith AM, Koo MS, DeFreitas AA, Zhang H, Kaplan G, Watowich SS, Murray PJ. Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling. Science Signaling. 2010 Aug 17;3(135):ra62.

El Kasmi KC, Qualls JE (co-primary author), Pesce JT, Smith AM, Thompson RW, Henao-Tamayo M, Basaraba RJ, König T, Schleicher U, Koo M, Kaplan G, Fitzgerald KA, Tuomanen EI, Orne IM, Kanneganti T, Bogdan C, Wynn TA, Murray PJ. TLR-induced Arginase 1 thwarts effective immunity against intracellular pathogens. Nature Immunology. 2008 Dec;9(12):1399-406.

L-citrulline and anti-tuberculosis host defense. Principal Investigator. National Institutes of Health/National Institute of Allergy and Infectious Diseases. July 2016-June 2021.

A photo of Nancy Ratner.

Nancy Ratner, PhD Co-Director, Rasopathy Program

Nancy Ratner, PhD, is working to define the interactions between glial cells and axons during nervous system development and how those interactions go awry in disease. Her goal is to develop novel therapies for patients with nervous system diseases.

Visit the Ratner Lab.

513-636-9469 nancy.ratner@cchmc.org

A photo of Nancy Ratner.

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Nancy Ratner, PhD

Co-Director, Rasopathy Program

Program Leader, Cancer Biology and Neural Tumors Program

Beatrice C. Lampkin Chair, Cancer Biology

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-9469

Fax 513-636-3549

Email nancy.ratner@cchmc.org

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Clinical & Research Interests

Clinical/Translational

Preclinical testing in neurofibromatosis tumors

Research

Genetic mutations in tumor suppressor genes; development of the nervous system; peripheral nerve tumor formation

Visit the Ratner Lab.

Nancy Ratner, PhD, is interested in understanding mechanisms of peripheral nerve tumor (neurofibroma) formation in neurofibromatosis type 1 (NF1), a common inherited disorder in which children are predisposed to cancer of the nervous system, to learning problems, bone disorders, and other cancers. She identified EGFR and MEK as potential therapeutic targets in NF1 peripheral nerve tumorigenesis, and has developed cell culture and mouse models of NF1 nerve tumorigenesis. Her laboratory has also used analysis of gene expression to identify critical genes in neurofibroma and their malignant derivatives, MPNST.

Dr. Ratner received her bachelor's from Brown University, her doctorate from Indiana University, and was a postdoctoral fellow at Washington University in St. Louis. She was a member of the faculty at the University of Cincinnati from 1987 to 2004. Dr. Ratner is currently a professor in the Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati, and the program leader for Cancer Biology and Neural Tumors Program in the Cancer and Blood Diseases Institute where she holds the Beatrice C. Lampkin Endowed chair in cancer biology and serves as PI of the NINDS P50 “Cincinnati Center in NF Research.”

Dr. Ratner is an active member of the International Consortium on the Molecular Biology of NF1, NF2, and Schwannomatosis and was a member of the advisory board for the National Neurofibromatosis Foundation (now Children’s Tumor Foundation) from 1989 to 2007. She chaired the Department of Defense Neurofibromatosis Research Program Integration Panel in 2008, and currently serves as a member of the James McDonnell Brain Tumor Research Advisory Board. She received the von Recklinghausen Award from the Children’s Tumor Foundation in 2010 and the Jacob K. Javits Neuroscience Investigator Award (NIH-NINDS MERIT Award) in 2014.

Education and Training

PhD: Indiana University, 1982.

BA: Brown University, 1975.

Fellowship: Washington University St. Louis, 1982-1987.

View PubMed Publications

Mitogenic Activities in Neurofibromatosis. Principal Investigator. Sept 2011-2016. NIH-R01 NS 28840-20.

Preclinical Testing: GEM-Neurofibroma. Principal Investigator. Children's Tumor Foundation. Aug 2013-Jul 2016.

Identification of Neurofibroma Growth and Drug Resistance Pathways. Principal Investigator. Neurofibromatosis Therapeutic Acceleration Program (NTAP). Apr 2014-Mar 2016.

Ras Proteins in Nerve Tumorigenesis. Principal Investigator. Apr 2014-Mar 2019. 1R01 NS083580-01A1.

Novel Combinatorial Therapies for Malignant Peripheral Nerve Sheath Tumors. Co-Principal Investigator. Jul 2014-Jun 2016. 1R21NS084885-01A1.

Disordered Wnt/b-catenin signaling in MPNST Development and Maintenance. Co-Principal Investigator. Oct 2014-Sep 2019. 1R01NS086219-01A1.

Can targeted therapy prevent neurofibroma growth in mice? Principal Investigator. Neurofibromatosis Therapeutic Acceleration Program (NTAP). Sep 2014-Aug 2016.

A photo of William Ridgway.

William Ridgway, MD

research investigates autoimmunity, immunogenetics, T cells, autoimmune (type I) diabetes, autoimmune liver disease (primary biliary cirrhosis), and relapsing polychondritis. The goal of the Ridgway Lab is to determine the immunogenetic mechanisms of autoimmune biliary disease, type one diabetes, and relapsing polychondritis arising in nonobese diabetic (NOD) and NOD congenic mice.

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513-558-4701 william.ridgway@uc.edu

A photo of William Ridgway.

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William Ridgway, MD

Academic Affiliations

Professor, UC Department of Internal Medicine

Phone 513-558-4701

Email william.ridgway@uc.edu

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Autoimmunity; immunogenetics; T cells; T regulatory cells; type 1 diabetes; autoimmune biliary disease

Education and Training

MD: University of Rochester, Rochester, NY.

Fellowship: Stanford University Medical Center, Stanford, CA.

View PubMed Publications

Yang GX, Wu Y, Tsukamoto H, Leung PS, Lian ZX, Rainbow DB, Hunter KM, Morris GA, Lyons PA, Peterson LB, Wicker LS, Gershwin ME, Ridgway WM. CD8 T cells mediate direct biliary ductule damage in nonobese diabetic autoimmune biliary disease. J Immunol. 2011 Jan 15;186(2):1259-67.

Ridgway WM, Peterson LB, Todd JA, Rainbow DB, Healy B, Burren OS, Wicker LS. Gene-gene interactions in the NOD mouse model of type 1 diabetes. Adv Immunol. 2008;100:151-75.

Irie J, Reck B, Wu Y, Wicker LS, Howlett S, Rainbow D, Feingold E, Ridgway WM. Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes. J Immunol. 2008 Jan 15;180(2):1071-9.

Irie J, Wu Y, Sass DA, Ridgway WM. Genetic control of anti-Sm autoantibody production in NOD congenic mice narrowed to the Idd9.3 region. Immunogenetics. 2006 Feb;58(1):9-14.

Koarada S, Wu Y, Fertig N, Sass DA, Nalesnik M, Todd JA, Lyons PA, Fenyk-Melody J, Rainbow DB, Wicker LS, Peterson LB, Ridgway WM. Genetic control of autoimmunity: protection from diabetes, but spontaneous autoimmune biliary disease in a nonobese diabetic congenic strain. J Immunol. 2004 Aug 15;173(4):2315-23.

Koarada S, Wu Y, Olshansky G, Ridgway WM. Increased nonobese diabetic Th1:Th2 (IFN-gamma:IL-4) ratio is CD4+ T cell intrinsic and independent of APC genetic background. J Immunol. 2002 Dec 1;169(11):6580-7.

Koarada S, Wu Y, Ridgway WM. Increased entry into the IFN-gamma effector pathway by CD4+ T cells selected by I-Ag7 on a nonobese diabetic versus C57BL/6 genetic background. J Immunol. 2001 Aug 1;167(3):1693-702.

Fassò M, Anandasabapathy N, Crawford F, Kappler J, Fathman CG, Ridgway WM. T cell receptor (TCR)-mediated repertoire selection and loss of TCR vbeta diversity during the initiation of a CD4(+) T cell response in vivo. J Exp Med. 2000 Dec 18;192(12):1719-30.

Ridgway WM, Fassò M, Fathman CG. A new look at MHC and autoimmune disease. Science. 1999 Apr 30;284(5415):749, 751.

Ridgway WM, Ito H, Fassò M, Yu C, Fathman CG. Analysis of the role of variation of major histocompatibility complex class II expression on nonobese diabetic (NOD) peripheral T cell response. J Exp Med. 1998 Dec 21;188(12):2267-75.

A photo of Marc Rothenberg.

Marc E. Rothenberg, MD, PhD Director, Division of Allergy and Immunology

Marc E. Rothenberg, MD, PhD, is focused on elucidating mechanisms of allergic responses, especially in mucosal tissues such as the lung and the gastrointestinal tract, in order to identify novel pharmaceutical targets for treatment of patients with eosinophilic diseases including eosinophilic gastrointestinal disorders, hypereosinophilic syndromes and asthma and food allergies. His lab has identified and characterized several critical pathways that regulate allergic responses.

Visit the Rothenberg Lab website.

513-803-0257 marc.rothenberg@cchmc.org

A photo of Marc Rothenberg.

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Marc E. Rothenberg, MD, PhD

Director, Division of Allergy and Immunology

Director, Cincinnati Center for Eosinophilic Disorders

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-0257

Fax 513-636-3310

Email marc.rothenberg@cchmc.org

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Clinical & Research Interests

Clinical

Eosinophilia; eosinophilic disorders; asthma; allergy; food allergy

Research

Eosinophils; chemokines

Visit the Rothenberg Lab.

Dr. Rothenberg is director of the Division of Allergy and Immunology at Cincinnati Children's Hospital Medical Center and tenured professor of pediatrics at Cincinnati Children’s within the University of Cincinnati College of Medicine. He graduated summa cum laude with highest honors in chemistry and biochemistry from Brandeis University. He then completed the MD/PhD program at Harvard Medical School under Dr. Frank Austen, conducting studies on eosinophil hematopoiesis, as he developed the first culture system for human eosinophils. After completing residency at Children’s Hospital, Boston, Dr. Rothenberg did a fellowship in allergy/immunology and hematology at Children’s Hospital. Dr. Rothenberg did post-doctorate training with Dr. Philip Leder, Harvard Medical School, where he cloned the eotaxin chemokine. After being faculty at Harvard Medical School for one year, he came to the University of Cincinnati and Cincinnati Children's, where he has helped build a top program in research, and his division is a leader in allergy and immunology.

His research is focused on molecular analysis of allergic inflammation, primarily on the molecular pathogenesis of eosinophilic esophagitis. His laboratory takes a multi-disciplinary approach including the development of preclinical murine models: genetics, genomics, molecular immunology, and biochemistry. Dr. Rothenberg’s awards include the 2007 E Mead Johnson Award from the Society of Pediatric Research, 2010 National Institutes of Health MERIT Award, and being elected an American Association for the Advancement of Science fellow. He is a member of the American Society for Clinical Investigation, American Academy of Pediatrics, and Society for Pediatric Radiology. His publications number over 300. He has served on review panels for journals/grant agencies including National Institutes of Health (NIH), Burroughs Trust, and Medical Research Council of the United Kingdom. He served for four years on the Advisory Council of National Institute of Allergy and Infectious Disease. He has been associate editor of the Journal of Allergy and Clinical Immunology since 2004. His research has been supported by sources including the NIH, Human Frontier Science Program Organization, Burroughs Wellcome Fund, Dana Foundation, and Department of Defense.

Visit the Rothenberg Lab website.

Education and Training

MD, PhD: Harvard Medical School, Cambridge, MA, 1990.

Residency: Pediatrics, Children's Hospital, Boston, MA, 1991-1992.

Fellowship: Immunology / Allergy, Children's Hospital, Boston, MA, 1992-1994; Hematology / Oncology, Children's Hospital and Dana Farber Cancer Institute, Boston, MA, 1992-1995.

Certification: National Board of Medical Examiners, 1991; Board of Registration in Medicine, MA, 1992; American Board of Pediatrics, 1995, 2001, 2008; Ohio State Medical Board, 1997; American Board of Allergy and Immunology, 1997, 2006.

Butz BK, Wen T, Gleich GJ, Furuta GT, Spergel J, King E, Kramer RE, Collins MH, Stucke E, Mangeot C, Jackson WD, O'Gorman M, Abonia JP, Pentiuk S, Putnam PE, Rothenberg ME. Efficacy, dose reduction, and resistance to high-dose fluticasone in patients with eosinophilic esophagitis. Gastroenterology. 2014 Aug;147(2):324:33.e5.

Sherrill JD, Kc K, Wu D, Djukic Z, Caldwell JM, Stucke EM, Kemme KA, Costello MS, Mingler MK, Blanchard C, Collins MH, Abonia JP, Putnam PE, Dellon ES, Orlando RC, Hogan SP, Rothenberg ME. Desmoglein-1 regulates esophageal epithelial barrier function and immune responses in eosinophilic esophagitis. Mucosal Immunol. 2014 May;7(3):718-29.

Wen T, Stucke EM, Grotjan TM, Kemme KA, Abonia JP, Putnam PE, Franciosi JP, Garza JM, Kaul A, King EC, Collins MH, Kushner JP, Rothenberg ME. Molecular diagnosis of eosinophilic esophagitis by gene expression profiling. Gastroenterology. 2013 Dec;145(6):1289-99.

Wen T, Besse JA, Mingler MK, Fulkerson PC, Rothenberg ME. Eosinophil adoptive transfer system to directly evaluate pulmonary eosinophil trafficking in vivo. Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):6067-72.

Lu TX, Sherrill JD, Wen T, Plassard AJ, Besse JA, Abonia JP, Franciosi JP, Putnam PE, Eby M, Martin LJ, Aronow BJ, Rothenberg ME. MicroRNA signature in patients with eosinophilic esophagitis, reversibility with glucocorticoids, and assessment as disease biomarkers. J Allergy Clin Immunol. 2012 Apr;129(4):1064-75.e9.

Rothenberg ME, Spergel JM, Sherrill JD, Annaiah K, Martin LJ, Cianferoni A, Gober L, Kim C, Glessner J, Frackelton E, Thomas K, Blanchard C, Liacouras C, Verma R, Aceves S, Collins MH, Brown-Whitehorn T, Putnam PE, Franciosi JP, Chiavacci RM, Grant SF, Abonia JP, Sleiman PM, Hakonarson H. Common variants at 5q22 associate with pediatric eosinophilic esophagitis. Nat Genet. 2010 Apr;42(4):289-91.

Rothenberg ME, Klion AD, Roufosse FE, Kahn JE, Weller PF, Simon HU, Schwartz LB, Rosenwasser LJ, Ring J, Griffin EF, Haig AE, Frewer PI, Parkin JM, Gleich GJ; Mepolizumab HEC Study Group. Treatment of patients with the hypereosinophilic syndrome with mepolizumab. N Engl J Med. 2008 Mar 20;358(12):1215-28.

Blanchard C, Wang N, Stringer KF, Mishra A, Fulkerson PC, Abonia JP, Jameson SC, Kirby C, Konikoff MR, Collins MH, Cohen MB, Akers R, Hogan SP, Assa'ad AH, Putnam PE, Aronow BJ, Rothenberg ME. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest. 2006 Feb;116(2):536-47.

Hogan SP, Mishra A, Brandt EB, Royalty MP, Pope SM, Zimmermann N, Foster PS, Rothenberg ME. A pathological function for eotaxin and eosinophils in eosinophilic gastrointestinal inflammation. Nat Immunol. 2001 Apr;2(4):353-60.

Mishra A, Hogan SP, Brandt EB, Rothenberg ME. An etiological role for aeroallergens and eosinophils in experimental esophagitis. J Clin Invest. 2001 Jan;107(1):83-90.

NICHHD Pediatric Center for Gene Expression and Developmental Sciences. Training Director. National Institutes of Health. Dec 2011–Nov 2016. K12 HD028827.

Epithelial Genes in Allergic Inflammation. Co-Investigator. National Institutes of Health. Sep 2011–Aug 2016. U19 AI070235.

Eosinophil:M2 Macrophage:CCL11 Axis in Experimental Colitis and Pediatric Corticosteroid Resistant Ulcerative Colitis. Co-Investigator. National Institutes of Health. Apr 2012–Mar 2016. R01 DK090119-01A1.

The Expression and Function of Paired Immunoglobulin-like Receptor B in Eosinophils. Co-Principal Investigator. U.S. - Israel Binational Science Foundation. Oct 2012–Sep 2016. #201144.

A photo of Paul Spearman.

Paul Spearman, MD Director, Division of Infectious Diseases

Paul Spearman, MD, directs a laboratory engaged in uncovering basic aspects of HIV-host cell interactions and the mechanisms of HIV transmission. We are also developing novel HIV vaccine strategies. Trafficking of the HIV-1 envelope glycoprotein, restriction of HIV spread by BST2/tetherin, and HIV infection of macrophages are areas of active investigation.

513-636-4509 paul.spearman@cchmc.org

A photo of Paul Spearman.

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Paul Spearman, MD

Director, Division of Infectious Diseases

Academic Affiliation

Professor

Phone 513-636-4509

Email paul.spearman@cchmc.org

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Clinical & Research Interests

Clinical

Pediatric infectious diseases

Research

HIV assembly; HIV biology/pathogenesis; HIV vaccines; vaccines and therapeutics for children (clinical trials)

Paul Spearman, MD is the Albert B. Sabin professor and director of Infectious Diseases at Cincinnati Children’s Hospital Medical Center. His laboratory studies fundamental aspects of HIV biology and develops new vaccines for human pathogens. HIV assembly processes are a major focus of the laboratory, including the trafficking of the HIV envelope glycoprotein and its interaction with essential host factors. A related project studies the role of tetherin in restricting HIV replication, and is defining how the viral protein Vpu counteracts this important host restriction factor. A novel mucosal HIV vaccine based on parainfluenza virus type 5 (PIV5) priming and virus-like particle boosting is under evaluation in macaque models. Dr. Spearman and his colleagues are engaged in the design and performance of clinical trials for new vaccines in adults and children, with a special interest in employing cutting-edge technologies to define innate and adaptive immune responses to vaccines.

Before moving to Cincinnati, Dr. Spearman was professor and vice chair for research in the Department of Pediatrics at Emory University, and chief research officer for Children’s Healthcare of Atlanta. While there he also served as co-director of the Emory Vaccine and Treatment Evaluation Unit (VTEU). Dr. Spearman currently serves on the Board of Scientific Counselors for NCI, frequently serves on study sections for NIAID, and is president-elect of the Pediatric Infectious Diseases Society (PIDS). Beyond his research interests, Dr. Spearman is a pediatric ID clinician and enjoys caring for children and mentoring future leaders in Infectious Diseases.

Education and Training

MD: University of Texas Southwestern, Dallas, TX, 1986.

Residency: Internal Medicine/Pediatrics, Ohio State University, Columbus, OH, 1986-1990.

Fellowship: Infectious Diseases, Washington University, St. Louis, MO, 1990-1993.

View PubMed Publications

Qi M, Chu H, Chen X, Choi J, Wen X, Hammonds J, Ding L, Hunter E, Spearman P. A tyrosine-based motif in the HIV-1 envelope glycoprotein tail mediates cell-type- and Rab11-FIP1C-dependent incorporation into virions. Proc Natl Acad Sci USA. 2015;112(24):7575-80.

Strauss JD, Hammonds JE, Yi H, Ding L, Spearman P, Wright ER. Three-Dimensional Structural Characterization of HIV-1 Tethered to Human Cells. J Virol. 2015;90(3):1507-21.

Wen X, Ding L, Wang JJ, Qi M, Hammonds J, Chu H, Chen X, Hunter E, Spearman P. ROCK1 and LIM kinase modulate retrovirus particle release and cell-cell transmission events. J Virol. 2014;88(12):6906-21.

Qi M, Williams JA, Chu H, Chen X, Wang JJ, Ding L, Akhirome E, Wen X, Lapierre LA, Goldenring JR, Spearman P. Rab11-FIP1C and Rab14 direct plasma membrane sorting and particle incorporation of the HIV-1 envelope glycoprotein complex. PLoS Pathog. 2013;9(4):e1003278.

Chu H, Wang JJ, Qi M, Yoon JJ, Chen X, Wen X, Hammonds J, Ding L, Spearman P. Tetherin/BST-2 Is Essential for the Formation of the Intracellular Virus-Containing Compartment in HIV-Infected Macrophages. Cell Host & Microbe. 2012;12(3):360-72.

Hammonds J, Ding L, Chu H, Geller K, Robbins A, Wang JJ, Yi H, Spearman P. The tetherin/BST-2 coiled-coil ectodomain mediates plasma membrane microdomain localization and restriction of particle release. J Virol. 2012;86(4):2259-72.

Spearman P, Lally MA, Elizaga M, Montefiori D, Tomaras GD, McElrath MJ, Hural J, De Rosa SC, Sato A, Huang Y, Frey SE, Sato P, Donnelly J, Barnett S, Corey LJ; HIV Vaccine Trials Network of NIAID. A trimeric, V2-deleted HIV-1 envelope glycoprotein vaccine elicits potent neutralizing antibodies but limited breadth of neutralization in human volunteers. J Infect Dis. 2011;203(8):1165-73.

Hammonds J, Wang JJ, Yi H, Spearman P. Immunoelectron microscopic evidence for Tetherin/BST2 as the physical bridge between HIV-1 virions and the plasma membrane. PLoS Pathog. 2010;6(2):e1000749.

Spearman P, Kalams S, Elizaga M, Metch B, Chiu YL, Allen M, Weinhold KJ, Ferrari G, Parker SD, McElrath MJ, Frey SE, Fuchs JD, Keefer MC, Lubeck MD, Egan M, Braun R, Eldridge JH, Haynes BF, Corey L; NIAID HIV Vaccine Trials Network. Safety and immunogenicity of a CTL multiepitope peptide vaccine for HIV with or without GM-CSF in a phase I trial. Vaccine. 2009;27(2):243-249.

Dong X, Li H, Derdowski A, Ding L, Burnett A, Chen X, Peters TR, Dermody TS, Woodruff E, Wang JJ, Spearman P. AP-3 directs the intracellular trafficking of HIV-1 Gag and plays a key role in particle assembly. Cell. 2005;120(5):663-74.

Viral and Cellular Determinants of HIV-1 Assembly. Principal Investigator. National Institutes of Health/National Institute of General Medical Sciences. Sep 2013-Aug 2017.

Mucosal Protection against HIV Generated by PIV5 Priming and VLP Boosting. Principal Investigator. National Institutes of Health/National Institute of Allergy and Infectious Diseases. Apr 2014-Mar 2018.

Role of Vpu in Retroviral Particle Assembly. Principal Investigator. National Institutes of Health/National Institute of Allergy and Infectious Diseases. Dec 2003-Nov 2016.

A photo of Daniel Starczynowski.

Daniel T. Starczynowski, PhD Member, Experimental Hematology and Cancer Biology

Daniel T. Starczynowski, PhD, is a cancer biologist who has a basic research programs with a translational emphasis in myeloid hematological malignancies. His lab’s major effort is studying the molecular and cellular basis of myelodysplastic syndromes, bone marrow failure syndromes and acute leukemia. The goal is to identify candidate genes and understand their contribution to myeloid malignancies.
Visit the Starczynowski Lab.

513-803-5317 daniel.starczynowski@cchmc.org

A photo of Daniel Starczynowski.

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Daniel T. Starczynowski, PhD

Member, Experimental Hematology and Cancer Biology

Co-Leader, Program in Hematologic Malignancies of Cincinnati Children's Hospital Medical Center, Cancer and Blood Diseases Institute

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-803-5317

Email daniel.starczynowski@cchmc.org

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Research Interests

Visit the Starczynowski Lab.

Daniel T. Starczynowski, PhD, received his PhD in molecular biology from Boston University. He studied the NF-kB family of transcription factors and their role in B-cell lymphomas. During his postdoctoral fellowship at the BC Cancer Research Center, Dr. Starczynowski identified and characterized novel candidate genes in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).

Following his postdoctoral training, Dr. Starczynowski joined the faculty at Cincinnati Children’s Hospital Medical Center and at the University of Cincinnati as an Assistant Professor. Dr. Starczynowski’s laboratory investigates the molecular and cellular basis of hematologic malignancies with the goal to advance novel therapeutic strategies.

Education and Training

BS: Fairleigh Dickinson University, Teaneck, NJ, 2000.

PhD: Boston University, Boston, MA, 2006.

Postdoctoral Fellow: University of British Columbia/BC Cancer Research Centre, Vancouver, Canada, 2010.

View PubMed Publications

A photo of Susan Thompson.

Susan Thompson, PhD

leads a translational research program dedicated to identifying juvenile idiopathic arthritis (JIA) genetic risk factors and disease-specific gene expression patterns to help understand the causes of JIA and the mechanisms of disease pathogenesis. This work has the long-term goal of developing molecular definitions of disease that can be used to improve diagnosis and response to therapy in JIA.
Visit the Thompson Lab.

513-636-3899 susan.thompson@cchmc.org

A photo of Susan Thompson.

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Susan Thompson, PhD

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-3899

Fax 513-636-3328

Email susan.thompson@cchmc.org

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Research Interests

Molecular basis of juvenile rheumatoid arthritis; large-scale integrative analysis of gene expression, polymorphism and other genomic data with clinical data

Visit the Thompson Lab.

Susan Thompson, PhD, has research interests that span both genetic and functional genomic studies of juvenile rheumatoid arthritis (JRA) to advance the understanding of the causes and mechanisms of disease pathogenesis. A genome-wide screen for JRA susceptibility traits has been completed and defined several regions for linkage mapping and candidate gene analysis. In addition, complementary approaches that measure global gene expression patterns using DNA microarrays are also being used to understand the molecular basis for disease.

Education and Training

PhD: University of Tennessee Center for Health Sciences, Memphis, TN, 1988.

Fellowship: Immunology, St. Jude Children's Research Hospital, Memphis, TN, 1988-1991.

Fellowship: Molecular Genetics, University of Cincinnati, Cincinnati, OH, 1991-1994.

View PubMed Publications

Thompson SD, Sudman M, Ramos PS, Marion MC, Ryan M, Tsoras M, Weiler T, Wagner M, Keddache M, Haas JP, Mueller C, Prahalad S, Bohnsack J, Wise CA, Punaro M, Zhang D, Rosé CD, Comeau ME, Divers J, Glass DN, Langefeld CD. The susceptibility loci juvenile idiopathic arthritis shares with other autoimmune diseases extend to PTPN2, COG6, and ANGPT1. Arthritis Rheum. 2010 Nov;62(11):3265-76.

Barnes MG, Grom AA, Thompson SD, Griffin TA, Luyrink LK, Colbert RA, Glass DN. Biologic similarities based on age at onset in oligoarticular and polyarticular subtypes of juvenile idiopathic arthritis. Arthritis Rheum. 2010 Nov;62(11):3249-58.

Thompson SD, Barnes MG, Griffin TA, Grom AA, Glass DN. Heterogeneity in juvenile idiopathic arthritis: impact of molecular profiling based on DNA polymorphism and gene expression patterns. Arthritis Rheum. 2010 Sep;62(9):2611-5.

Hinze CH, Fall N, Thornton S, Mo JQ, Aronow BJ, Layh-Schmitt G, Griffin TA, Thompson SD, Colbert RA, Glass DN, Barnes MG, Grom AA. Immature cell populations and an erythropoiesis gene-expression signature in systemic juvenile idiopathic arthritis: implications for pathogenesis. Arthritis Res Ther. 2010;12(3):R123.

Barnes MG, Grom AA, Thompson SD, Griffin TA, Pavlidis P, Itert L, Fall N, Sowders DP, Hinze CH, Aronow BJ, Luyrink LK, Srivastava S, Ilowite NT, Gottlieb BS, Olson JC, Sherry DD, Glass DN, Colbert RA. Subtype-specific peripheral blood gene expression profiles in recent-onset juvenile idiopathic arthritis. Arthritis Rheum. 2009 Jul;60(7):2102-12.

Griffin TA, Barnes MG, Ilowite NT, Olson JC, Sherry DD, Gottlieb BS, Aronow BJ, Pavlidis P, Hinze CH, Thornton S, Thompson SD, Grom AA, Colbert RA, Glass DN. Gene expression signatures in polyarticular juvenile idiopathic arthritis demonstrate disease heterogeneity and offer a molecular classification of disease subsets. Arthritis Rheum. 2009 Jul;60(7):2113-23.

Zhang K, Biroschak J, Glass DN, Thompson SD, Finkel T, Passo MH, Binstadt BA, Filipovich A, Grom AA. Macrophage activation syndrome in patients with systemic juvenile idiopathic arthritis is associated with MUNC13-4 polymorphisms. Arthritis Rheum. 2008 Sep;58(9):2892-6.

Chaudhari M, Moroldo MB, Shear E, Hillard P, Thompson SD, Lan D, Huang B, Brunner HI, Glass DN. Impaired reproductive fitness in mothers of children with juvenile autoimmune arthropathies. Rheumatology (Oxford). 2006 Oct;45(10):1282-7.

Phelan JD, Thompson SD. Genomic progress in pediatric arthritis: recent work and future goals. Curr Opin Rheumatol. 2006 Sep;18(5):482-9.

Phelan JD, Thompson SD, Glass DN. Susceptibility to JRA/JIA: complementing general autoimmune and arthritis traits. Genes Immun. 2006 Jan;7(1):1-10.

A photo of Stephen Waggoner.

Stephen N. Waggoner, PhD

is a viral immunologist whose lab studies immune regulatory mechanisms that control pathogenesis of disease. The lab uses viruses and bacteria to probe immune functions associated with disease in mice. Interests currently focus on a novel regulatory role of natural killer (NK) cells that influences vaccine efficacy, autoimmune disease, chronic viral infections, and immune dysfunction in the elderly.

513-803-4607 stephen.waggoner@cchmc.org

A photo of Stephen Waggoner.

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Stephen N. Waggoner, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-803-4607

Email stephen.waggoner@cchmc.org

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Research Interests

Viral immunology; natural killer cells; immunoregulation; vaccines; autoimmunity; immune dysfunction in aging.

Visit the Waggoner Lab.

Stephen Waggoner, PhD, is an assistant professor in the Center for Autoimmune Genomics and Etiology (CAGE) within the Division of Rheumatology at Cincinnati Children's Hospital Medical Center within the UC Department of Pediatrics. Dr. Waggoner received his PhD from the University of Virginia, conducted postdoctoral research at the University of Massachusetts Medical School, and joined the faculty at Cincinnati Children’s in 2013. He has garnered international recognition for his discovery that natural killer (NK) cells play a crucial regulatory role during persistent virus infection involving suppression of virus-specific T cell responses. His lab continues to explore the relevance of this phenomenon to chronic infection, vaccine efficacy, autoimmune disease, and age-associated immune dysfunction.

Education and Training

BA: St. Mary's College of Maryland, St. Mary's City, MD, 2000.

PhD: University of Virginia, Charlottesville, VA, 2007.

Post Doc: University of Massachusetts Medical School, Worcester, MA.

View PubMed Publications

Severa M, Islam SA, Waggoner SN, Jiang Z, Kim ND, Ryan G, Kurt-Jones E, Charo I, Caffrey DR, Boyartchuk VL, Luster AD, Fitzgerald KA. The transcriptional repressor BLIMP1 curbs host defenses by suppressing expression of the chemokine CCL8. The Journal of Immunology. 2014; 192(5):2291-304.

Waggoner SN, Daniels KA, Welsh RM. Therapeutic depletion of natural killer cells controls persistent infection. Journal of Virology. 2014; 88(4):1953-60.

Cornberg M, Kenney LL, Chen AT, Waggoner SN, Kim SK, Dienes HP, Welsh RM, Selin LK. Clonal exhaustion as a mechanism to protect against severe immuno-pathology and death from an overwhelming CD8 T cell response. Frontiers in Immunology. 2013; 4:475.

Welsh RM, Waggoner SN. NK cells controlling virus-specific T cells: Rheostats for acute vs. persistent infections. Virology. 2013; 435(1):37-45. Review.

Waggoner SN, Kumar V. Evolving role of 2B4/CD244 in T and NK cell responses during virus infection. Frontiers in Immunology. 2012; 3:377. Review.

Waggoner SN, Cornberg M, Selin LK, Welsh RM. Natural killer cells act as rheostats modulating anti-viral T cells. Nature. 2011; 481(7381):394-398.
This paper is “Faculty of 1000 recommended.”

Rathinam VA, Jiang Z, Waggoner SN, Sharma S, Cole LE, Waggoner L, Vanaja SK, Monks BG, Ganesan S, Latz E, Hornung V, Vogel SN, Szomolanyi-Tsuda E, Fitzgerald KA. The AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses. Nature Immunology. 2010; 11(5):395-402.
This paper is “Faculty of 1000 recommended.”

Waggoner SN, Taniguchi RT, Mathew PA, Kumar V, Welsh RM. Absence of mouse 2B4 promotes NK cell–mediated killing of activated CD8+ T cells, leading to prolonged viral persistence and altered pathogenesis. Journal of Clinical Investigation. 2010; 120(6): 1925-38.

Waggoner SN, Hall CH, Hahn YS. HCV core protein interaction with gC1q receptor inhibits Th1 differentiation of CD4+ T cells via suppression of dendritic cell IL-12 production. Journal of Leukocyte Biology. 2007; 82(6):1407-1419.

Waggoner SN, Cruise MW, Kassel R, Hahn YS. gC1q receptor ligation selectively down-regulates human interleukin-12 production through activation of the phosphoinositide 3-kinase pathway. Journal of Immunology. 2005; 175(7):4706-4714.

Effect of aging on natural killer cell regulation of T cells in viral pathogenesis. Principal Investigator. Ellison Medical Foundation New Scholar in Aging. July 2012-July 2016.

A revolutionary vaccine approach to prevent HIV infection in substance abuse. Principal Investigator. National Institute on Drug Abuse (NIDA) Avant-Garde Award For HIV/AIDS Research. June 2014-May 2019.

A photo of Sing Sing Way.

Sing Sing Way, MD, PhD Pauline and Lawson Reed Chair, Division of Infectious Diseases

Sing Sing Way, MD, PhD, is an infectious disease physician-scientist. He cares for infants and children with infection related illness, and provides consultation in the diagnosis and prevention diseases caused by communicable agents. Dr. Way supervises an active basic research laboratory that uses basic immunological approaches to investigate ways to boost host defense and protection against infection. If you have interest in this work, please contact Dr. Way.

513-636-7603 singsing.way@cchmc.org

A photo of Sing Sing Way.

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Sing Sing Way, MD, PhD

Pauline and Lawson Reed Chair, Division of Infectious Diseases

Academic Affiliations

Associate Professor, UC Department of Pediatrics

Phone 513-636-7603

Email singsing.way@cchmc.org

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Infectious diseases; prenatal infection; immunology

Dr. Way is an infectious disease physician-scientist. He cares for infants and children with infection related illness, and provides consultation in the diagnosis and prevention diseases caused by communicable agents. Dr. Way supervises an active basic research laboratory that uses basic immunological approaches to investigate ways to boost host defense and protection against infection. Ongoing projects investigate the immune basis responsible for enhanced susceptibility to infection during pregnancy, the immune pathogenesis of pregnancy complications that occur with maternal infection, and the basic signals required for stimulating immune cell activation.

Dr. Way trained in the combined MD/PhD program at the Albert Einstein College of Medicine, pediatric residency at the University of California San Francisco, and infectious disease fellowship at the University of Washington. During fellowship training, Dr. Way began investigating the basic immunology and immune pathogenesis of infectious diseases relevant to human, and in particular, infant and child health.

Dr. Way’s research has been supported by the National Institutes of Health since 2006. Dr. Way’s research has been described in many publications in numerous prestigious scientific journals including Nature, Cell Host & Microbe, PLoS Pathogens, and The Journal of Immunology. The past and ongoing work has also been recognized by numerous prestigious awards including the Infectious Diseases Society of America Wyeth Young Investigator Award, a Basil O’ Conner Award from the March of Dimes Foundation, and the Investigator in Pathogenesis of Infectious Diseases award from the Burroughs Wellcome Fund.

Education and Training

MD PhD: Albert Einstein College of Medicine, Bronx, NY, 1999.

Residency: University of California San Francisco, San Francisco, CA, 2001.

Fellowship: University of Washington, Seattle, WA, 2004.

View PubMed Publications

Rowe JH, Ertelt JM, Xin L, Way SS. Pregnancy imprints regulatory memory that sustains anergy to fetal antigen. Nature. 490: 102-106. 2012.

Rowe JH, Ertelt JM, Xin L, Way SS. Listeria monocytogenes cytoplasmic entry induces fetal wastage by disrupting maternal Foxp3+ regulatory T cell-sustained fetal tolerance. PLoS Pathog. 8: e1002873. 2012.

Rowe JH, Ertelt JM, Way SS. Innate IFN-g is essential for Programmed death ligand-1-mediated T cell stimulation following Listeria monocytogenes infection. J Immunol. 189: 876-84. 2012.

Rowe JH, Ertelt JM, Way SS. Foxp3+ regulatory T cells, immune stimulation, and host defense against infection. Immunology. 136:1-10. 2011.

Ertelt JM, Johanns TM, Mysz MA, Nanton MR, Rowe JH, Aguilera MN, Way SS. Selective culling of high avidity antigen-specific CD4+ T cells after virulent Salmonella infection. Immunology. 134: 487-97. 2011.

Ertelt JM, Rowe JH, Mysz MA, Singh C, Roychowdhury M, Aguilera MN, Way SS. Foxp3+ regulatory T cells impede the priming of protective CD8+ T cells. J Immunol. 187: 2569-77. 2011.

Rowe JH, Ertelt JM, Aguilera MN, Farrar MA, Way SS. Foxp3+ regulatory T cell expansion required for sustaining pregnancy compromises host defense against prenatal bacterial pathogens. Cell Host Microbe. 10:54-64. 2011.

Johanns TM, Law CY, Kalekar LA, O’Donnell H, Ertelt JM, Rowe JH, Way SS. Early eradication of persistent Salmonella infection primes antibody-mediated protective immunity to recurrent infection. Microbes Infect. 13: 322-330. 2011.

Han JY, Hanson DC, Way SS. Herpes Zoster and meningitis due to reactivation of varicella vaccine virus in a immunocompetent child. Pediatr Infect Dis J. 30:266-268. 2011.

Ertelt JM, Johanns TM, Rowe JH, Way SS. IL-21-independent pathogen-specific CD8+ T cell expansion, and IL-21-dependnent suppression of CD4+ T cell IL-17 production. Immunology. 131: 183-191. 2010.

Maternal regulatory T cells control the immune pathogenesis of prenatal infection. Principal Investigator in the Pathogenesis of Infectious Disease. Burroughs Wellcome Fund. 2012-2017.

The immune pathogenesis of prenatal Listeria monocytogenes infection. Principal Investigator. National Institute of Allergy and Infectious Diseases (NIAID). 2012-2017. R01-AI100934.

A photo of Matthew Weirauch.

Matthew T. Weirauch, PhD

Matthew T. Weirauch, PhD, is a computational biologist. His lab seeks to understand the mechanisms of gene transcriptional regulation. Current projects focus on characterizing transcription factor binding specificities, and developing methods for modeling their interactions with DNA, both in vitro and in vivo. His lab applies insights from basic research on transcription factor-DNA interactions to study the mechanisms underlying complex diseases.

Visit the Weirauch Lab.

513-803-9078 matthew.weirauch@cchmc.org

A photo of Matthew Weirauch.

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Matthew T. Weirauch, PhD

Academic Affiliations

Assistant Professor, UC Department of Pediatrics

Phone 513-803-9078

Email matthew.weirauch@cchmc.org

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Transcription factors; transcriptional regulation; functional genomics; genome analysis

Visit the Weirauch Lab.

Dr. Weirauch is a computational biologist. His lab seeks to understand the mechanisms of gene transcriptional regulation. Current projects focus on characterizing transcription factor binding specificities, and developing methods for modeling their interactions with DNA, both in vitro and in vivo. His lab applies insights from basic research on transcription factor-DNA interactions to study the mechanisms underlying complex diseases.

Education and Training

Postdoctoral Fellow: University of Toronto (Donnelly Center for Cellular and Biomolecular Research), Toronto, Ontario, Canada.

PhD: Bioinformatics, University of California Santa Cruz, Santa Cruz, California.

BSc: Computer Science, Pennsylvania State University, University Park, PA.

View PubMed Publications

Alipanahi B, Delong A, Weirauch MT, Frey BJ. Predicting the sequence specificities of DNA- and RNA-binding proteins by deep learning. Nat Biotechnol. 2015 Aug;33(8):831-8.

Narasimhan K, Lambert SA, Yang AW, Riddell J, Mnaimneh S, Zheng H, Albu M, Najafabadi HS, Reece-Hoyes JS, Fuxman Bass JI, Walhout AJ, Weirauch MT, Hughes TR. Mapping and analysis of Caenorhabditis elegans transcription factor sequence specificities. Elife. 2015 Apr 23;4.

Weirauch M, Yang A, Albu M, Cote A, Montenegro-Montero A, Drewe P, Najafabadi H, Lambert S, Mann I, Cook K, Zheng H, Goity A, van Bakel H, Lozano J, Galli M, Lewsey M, Huang E, Mukherjee T, Chen X, Reece-Hoyes J, Govindarajan S, Shaulsky G, Walhout AJM, Bouget F, Ratsch G, Larrondo L, Ecker J, Hughes T. Determination and inference of eukaryotic transcription factor sequence specificity. Cell. 2014 Sep 11;158(6):1431-1443.

Ray D*, Kazan H*, Cook K*, Weirauch M*, Najafabadi H*, Li X, Gueroussov S, Albu M, Zheng H, Yang A, Na H, Irimia M, Matzat L, Dale R, Smith S, Yarosh C, Kelly S, Nabet B, Mecenas D, Li W, Laishram R, Qiao M, Lipshitz H, Piano F, Corbett A, Carstens R, Frey B, Anderson R, Lynch K, Penalva L, Lei E, Fraser A, Blencowe B, Morris Q, Hughes T. A compendium of RNA binding motifs for decoding gene regulation. Nature. 2013 Jul 10;499(7457):172-177. *co-first authors.

Weirauch M, Cote A, Norel R, Annala M, Zhao Y, Riley T, Saez-Rodriguez J, Cokelaer T, Vedenko A, Talukder S, DREAM5 Consortium, et al. Evaluation of methods for modeling transcription factor sequence specificity. Nature Biotechnology. 2013 Jan 27;31(2):126-34.

Viral transcription factor interactions with disease-associated genetic variants. Principal Investigator. Trustee Award, Cincinnati Children's. Jul 2014-Jun 2016.

Translational Genomics Analysis Core. Co-Investigator. NIH/NCRR CCTST T1 Pilot, Cincinnati Children's. Jul 2014-Jun 2016.

Decoding C2H2 Zinc Fingers. Collaborator. Canadian Institutes of Health Research (CIHR) Operating Grant. Oct 2013-Sep 2016.

A photo of Susanne Wells.

Susanne Wells, PhD Director, Epithelial Carcinogenesis and Stem Cell Program

Susanne Wells, PhD, focuses on new targets of the HPV E6/E7 oncogenes, and characterizing these as potential risk factors for HPV infection and transformation. Research approaches include bioinformatics; analyses of primary, transformed and 3D cell culture systems; and mouse tumor models to facilitate translational endeavors.
Visit the Wells Lab.

513-636-5986 susanne.wells@cchmc.org

A photo of Susanne Wells.

High Res

Susanne Wells, PhD

Director, Epithelial Carcinogenesis and Stem Cell Program

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-5986

Fax 513-636-3549

Email susanne.wells@cchmc.org

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Susceptibility to squamous cell carcinoma of the cervix, head and neck, esophagus, skin; induced pluripotent stem cell models to recapitulate the natural history of HPV infection and cancer development; mechanisms by which HPV oncogenes subvert the host cell machinery to promote abnormal metabolism, cellular growth and transformation; breast cancer signaling and metabolism

Visit the Wells Lab.

Susanne Wells graduated from the University of Konstanz, Germany, with a degree in Biology. She completed her PhD in Molecular Genetics and Microbiology at the State University of Stony Brook, NY, and her Postdoctoral Fellowship at Harvard Medical School, MA. Dr. Wells moved to Cincinnati Children's Hospital Medical Center in 2002 to study epithelial carcinogenesis and stem cells.

Education and Training

BS: Biology, University of Konstanz, Germany, 1992.

PhD: Molecular Genetics, State University of Stony Brook, NY, 1997.

Postdoctoral Fellowship: Molecular Virology, Harvard Medical School, Boston, MA.

View PubMed Publications

Strengthening epidermal defenses for the prevention of HPV infection and replication. Principal Investigator. National Institutes of Health. 2018-2023. R01 CA228113.

FA pathway activities in the normal and transformed epidermis. Principal Investigator. National Institutes of Health. 2018-2023. R01 CA223790.

Therapeutic target discovery in pediatric recurrent respiratory papillomatosis. Principal Investigator. National Institutes of Health. 2018-2020. R21 AI142704.

Improving the treatment of challenging FA cancers by proton precision therapy. Principal Investigator. Cancer Free Kids Grant. 2018-2020.

Proton Radiation Biology Discovery and Translation. Co-Principal Investigator. Academic and Research Committee Grant. 2017-2020.

A photo of Yi Zheng.

Yi Zheng, PhD Director, Experimental Hematology and Cancer Biology

Yi Zheng, PhD, studies the function and signaling mechanism of the Rho family GTPases and the mTor metabolic pathway, particularly in stem cell and cancer stem cell regulation.
Visit the Zheng Lab.

513-636-0595 yi.zheng@cchmc.org

A photo of Yi Zheng.

High Res

Yi Zheng, PhD

Director, Experimental Hematology and Cancer Biology

Institute Co-Director, Cancer and Blood Diseases Institute

Katherine Stewart Waters Endowed Chair

Academic Affiliations

Professor, UC Department of Pediatrics

Phone 513-636-0595

Fax 513-636-3768

Email yi.zheng@cchmc.org

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Research Interests

Using transgenic and gene targeted mouse models to study the physiological and pathological roles of Rho GTPases and their regulators in hematopoiesis, neurogenesis, lung cancer development and small intestinal stem cell regulations mechanism based, rational design of small molecule inhibitors targeting Rho GTPase signaling modules and pathologic functions in cancer and blood diseases; mouse model studies of mTor signaling function in hematopoietic stem cells and small intestinal stem cells.

Visit the Zheng Lab.

Education and Training

BS: Tsinghua University, Beijing, China, 1986.

MS: Cornell University, Ithaca, NY, 1988.

PhD: Cornell University, Ithaca, NY, 1991.

Postdoctoral Fellow: Cornell University, Ithaca, NY, 1995.

View All PubMed Publications

Maliken BD, Kanisicak O, Karch J, Khalil H, Fu X, Boyer JG, Prasad V, Zheng Y, Molkentin JD. Gata4-Dependent Differentiation of c-Kit+ Derived Endothelial Cells Underlies Artefactual Cardiomyocyte Regeneration in the Heart. Circulation. 2018 Apr 17.

Akbar H, Duan X, Piatt R, Saleem S, Davis AK, Tandon NN, Bergmeier W, Zheng Y. Small molecule targeting the Rac1-NOX2 interaction prevents collagen-related peptide and thrombin induced reactive oxygen species generation and platelet activation. J Thromb Haemost. 2018 Jul 14.

Liu W, Du W, Shang X, Wang L, Evelyn C, Florian MC, A Ryan M, Rayes A, Zhao X, Setchell K, Meller J, Guo F, Nassar N, Geiger H, Pang Q, Zheng Y. Rational identification of a Cdc42 inhibitor presents a new regimen for long-term hematopoietic stem cell mobilization. Leukemia. 2018 Sep 25.

Du W, Liu W, Mizukawa B, Shang X, Sipple J, Wunderlich M, Geiger H, Davies S, Mulloy J, Pang Q, Zheng Y. A non-myeloablative conditioning approach for long-term engraftment of human and mouse hematopoietic stem cells. Leukemia. 2018 Jun 29.

Grigoryan A, Guidi N, Senger K, Liehr T, Soller K, Marka G, Vollmer A, Markaki Y, Leonhardt H, Buske C, Lipka DB, Plass C, Zheng Y, Mulaw MA, Geiger H, Florian MC. LaminA/C regulates epigenetic and chromatin architecture changes upon aging of hematopoietic stem cells. Genome Biol. 2018 Nov 7;19(1):189.

Florian MC, Klose M, Sacma M, Jablanovic J, Knudson L, Nattamai KJ, Marka G, Vollmer A, Soller K, Sakk V, Cabezas-Wallscheid N, Zheng Y, Mulaw MA, Glauche I, Geiger H. Aging alters the epigenetic asymmetry of HSC division. PLoS Biol. 2018 Sep 20;16(9):e2003389.

Chadwick ML, Lane A, Thomas D, Smith AR, White AR, Davidson D, Feng Y, Boscolo E, Zheng Y, Adams DM, Gupta A, Veillette A, Chow LML. Combined mTOR and MEK inhibition is an effective therapy in a novel mouse model for angiosarcoma. Oncotarget. 2018 May 15;9(37):24750-24765.

Yang JQ, Kalim KW, Li Y, Duan X, Nguyen P, Khurana Hershey GK, Kroner J, Ruff B, Li Z, Salomonis N, Rochman M, Wen T, Zheng Y, Guo F. Rational targeting Cdc42 restrains Th2 cell differentiation and prevents allergic airway inflammation. Clin Exp Allergy. 2018 Oct 11.

Hayashi Y, Zhang Y, Yokota A, Yan X, Liu J, Choi K, Li B, Sashida G, Peng Y, Xu Z, Huang R, Zhang L, Freudiger GM, Wang J, Dong Y, Zhou Y, Wang J, Wu L, Bu J, Chen A, Zhao X, Sun X, Chetal K, Olsson A, Watanabe M, Romick-Rosendale LE, Harada H, Shih LY, Tse W, Bridges JP, Caligiuri MA, Huang T, Zheng Y, Witte DP, Wang QF, Qu CK, Salomonis N, Grimes HL, Nimer SD, Xiao Z, Huang G. Pathobiologic Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes. Cancer Discov. 2018 Aug 23.

Nayak R, Hegde S, Althoff M, Wellendorf A, Mohmoud F, Perentesis J, Reina-Campos M, Reynaud D, Zheng Y, Diaz-meco M, Moscat J, Cancelas JA. The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors. Nature Communications. 2018.

Targeting Cdc42 for bone marrow transplant therapies. Principal investigator. National Institutes of Health. Apr 2015 - Apr 2020. NIH R01CA193350.

Cdc42, hematopoietic stem cell polarity and cell fate. Principal Investigator. National Institute of Health - NIDDK. Dec 2015 - Nov 2019.

Blood stem cell aging and biomarker studies. Co-Principal Investigator. National Institute of Health - NHLBI. Aug 2016 - July 2020.

Activated protein C peptides for radio-mitigation. Co-Principal Investigator. National Institute of Health - NIAID. Apr 2017 - Mar 2019.

Leukemia Stem cell polarity and differentiation therapy. Co-Principal Investigator. National Institute of Health - NCI. Sep 2017 - July 2022.

Targeting TET1 signaling to treat acute myeloid leukemia. Co-Investigator. National Institutes of Health. Jan 2017 - Dec 2021. R01CA211614.

Refrigerated preservation of platelets for human transfusion. Co-Principal Investigator. Ohio Third Frontier Fund. Feb 2018 - Jan 2019.

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