Immunology Graduate Training Program

  • Meet the Faculty

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    Faculty

    A photo of Julio Aliberti.

    Julio Aliberti, MS, PhD

    is focused on defining the mechanisms underlying the induction and regulation of immune responses to intracellular pathogens, including Toxoplasma gondii and Mycobacterium tuberculosis, microbes that cause an immense burden of morbidity and mortality in the world at large. The ultimate goal of this research program is the development of novel preventive and therapeutic approaches to these pathogens.

    513-636-9041
    julio.aliberti@cchmc.org

    Julio Aliberti, MS, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-9041

    Fax: 513-636-5355

    Email: julio.aliberti@cchmc.org

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    Education and Training

    BSc: Biology, FFCL Barao de Maua, Ribeirao Preto, Brazil, 1994.

    MS: Immunology, FMRP / USP, Ribeirao Preto, Brazil, 1996.

    PhD: Immunology, FMRP / USP, Ribeirao Preto, Brazil, 1998.

    Publications

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    Grants

    Long-term Immunity Against Toxoplasmosis. Principal Investigator. National Institute of Allergy and Infectious Diseases. April 2008 – March 2013. #R01 AI033325.

    Control of immune responses by lipoxins during tuberculosis. Principal Investigator. National Institutes of Health. April 2008 – March 2013. #01AI075038.

    A photo of Dr. Artem Barski.

    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

    Artem Barski, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-1851

    Email: artem.barski@cchmc.org

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    Specialties

    Epigenetics; epigenomics; immunology; T cell memory

    Visit the Barski Lab

    Biography

    Artem Barski, PhD, is interested in epigenetic and transcriptional regulation of gene expression. 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. Together with his NIH colleagues Dr. Barski used this approach to map more than 40 chromatin modifications in human T cells, which fundamentally improved the understanding of epigenetic regulation of transcription. Dr. Barski has since been using ChIP-Seq and other sequencing-based genome-wide methods to understand the role of chromatin modifications in gene regulation. His most recent work includes investigation of chromatin regulation of genes transcribed by RNA Polymerase III and the discovery of gene poising in T cells.

    Since his arrival to Cincinnati Children’s Hospital Medical Center in 2011, Dr. Barski is utilizing ChIP-Seq, RNA-Seq and other cutting-edge approaches to understand epigenetic basis of T cell activation, memory and tolerance.

    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.

    Publications

    A photo of Jorge Bezerra.

    Jorge A. Bezerra, MD Medical Director, Pediatric Liver Care Center

    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

    Jorge A. Bezerra, MD

    Medical Director, Pediatric Liver Care Center

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-3008

    Fax: 513-636-5581

    Email: jorge.bezerra@cchmc.org

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    Specialties

    Biography

    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 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

    Publications

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    Charles C. Caldwell, PhD

    focuses his research around trauma, sepsis and inflammation.

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

    Charles C. Caldwell, PhD

    Academic Information

    Associate Professor, UC Department of Surgery

    Phone: 513-558-1974

    Email: caldwecs@ucmail.uc.edu

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    Education and Training

    BA: University of California, San Diego, CA. 

    PhD: San Diego State University, San Diego, CA. 

    Post-doctoral Studies: Laboratory of Immunology, NIAID, NIH

    A photo of Jose Cancelas Perez.

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

    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

    Jose A. Cancelas Perez, MD, PhD

    Division Director of Research, Hoxworth Blood Center

    Deputy Director, Hoxworth Blood Center

    Director, Research Flow Cytometry Core

    Leader, Stem Cell Program

    Medical Director of Cellular Therapies, Hoxworth Blood Center

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-558-1324

    Fax: 513-558-1522

    Email: jose.cancelas@uc.edu

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    Specialties

    Hematopoietic stem cell proliferation and differentiation

    Visit the Cancelas Lab.

    Education and Training

    MD: Autonomous University of Madrid, Spain, 1989.

    Residency: Hematology and Hematotherapy, University of Alcala de Henares, Madrid, Spain, 1993.

    PhD: Faculty of Medicine, University of Alcala de Henares, Madrid, Spain, 1996.

    Publications

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    Grants

    Progenitor Cell Biology Consortium Administrative Coordinating Center, NHLBI/ Subaward through Univ. Maryland. Co-Director. (Cincinnati Cell Char Core). Sep 2010 – Aug 2016. #U01 HL099997. 

    Rational Design of a Vav/Rac Inhibitor as a New Therapy for High-Risk B-ALL. Principal Investigator. Leukemia & Lymphoma Society of North America. Oct 2012 – Sep 2015. 

    Cincinnati Excellence in Molecular Hematology: Cell Analysis and Sorting Core, NIH/NIDDK. Co-investigator. (Flow Cytometry Core Co-PI).  Sep 2010 – Jun 2015. #P30DK090971-01.

    A photo of Claire Chougnet.

    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.

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

    Claire A. Chougnet, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-8847

    Fax: 513-636-4278

    Email: claire.chougnet@cchmc.org

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    Specialties

    Clinical Interests

    Antigen-presenting cells; HIV research; ontogeny of immune responses

    Research Interests

    HIV/AIDS pathogenesis; immune dysfunction in aging; ontogeny of immune system

    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.

    Publications

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    A photo of Jay Degen.

    Jay L. Degen, PhD

    studies the mechanisms by which circulating and cell-associated hemostatic factors contribute to development, tissue reorganization, inflammatory processes and disease. He also focuses on defining the regulatory pathways by which thrombin and thrombin targets contribute to cancer biology, inflammatory joint disease, neuroinflammatory disease, bacterial virulence/host defense, and immunological disorders.  

    513-636-4679
    jay.degen@cchmc.org

    Jay L. Degen, PhD

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-4679

    Email: jay.degen@cchmc.org

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    Specialties

    Molecular genetics of plasminogen activation in development, hemostasis, and tumor progression; molecular genetics and biological role of plasminogen activation in development, hemostasis, wound repair, and disease

    Biography

    Jay L. Degen, PhD, is studying the regulation and biological roles of urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA), the two mammalian enzymes that convert plasminogen to the active serine protease, plasmin.

    The PA/plasmin system of proteases is of particular interest because of its apparent dual function in the lysis of vascular fibrin clots (fibrinolysis) and the degradation of extracellular matrix in tissue remodeling and cell migration events. 

    Over the last few years, Dr. Degen's lab has generated and characterized gene-targeted mouse lines with deficits in the factors that are the foundation of the coagulation and fibrinolytic cascades, including fibrinogen-, plasminogen-, plasminogen activator-, and plasminogen activator receptor-deficient mouse lines.

    These unique experimental animals are being intensively analyzed with regard to a wide range of phenotypic properties, including hemostasis, wound healing, angiogenesis and tumor biology.

    Education and Training

    PhD: University of Washington, 1983. 

    Publications

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    Grants

    Thrombin-mediated proteolysis in neuroinflammatory disease. Principal Investigator. National Heart, Lung and Blood Institute. Jul 2009  – Jun 2014. #R01 HL096126.
    A photo of Senad Divanovic.

    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.

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

    Senad Divanovic, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-0286

    Email: senad.divanovic@cchmc.org

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    Specialties

    Innate immune responses; obesity; NAFLD; preterm birth

    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

    Publications

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    Grants

    Better mouse models of disease: Humanizing experimental atherosclerosis. Principal Investigator. NHLBI. Apr 2012 - Mar 2014.

    Endocannabinoid signaling via CB2 protects against preterm birth by modulating immune responses. Co-Investigator. March of Dimes, Prematurity Research Initiative Grant. Mar 2012 - Feb 2015.
    A photo of Marie-Dominique Filippi.

    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

    Marie-Dominique Filippi, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-0991

    Fax: 513-636-3768

    Email: Marie-Dominique.Filippi@cchmc.org

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    Biography

    Dr. Filippi is particularly interested in dissecting the molecular mechanism of hematopoietic cell migration, including neutrophils and hematopoietic stem cells in physiological settings. Migration is a critical function of hematopoietic cell in which actin cytoskeleton reorganization plays a central role. 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. The small RHO GTPase family, members of the Ras superfamily, including Rac, RHO and CDC42, play key roles in regulating many of these functions. During her post-doc in the laboratory of Dr. David Williams, they have demonstrated that two highly related proteins, Rac1 and Rac2, of the small Rho GTPase family, have distinct functions in the control of hematopoietic cell functions. In particular in neutrophils, they have shown that both Rac1 and Rac2 regulate cell migration but with distinct mechanism (Gu and Filippi et al, Science 2003) both in vitro and in vivo. In addition to this work, they have dissected the sequence/determinant specificity of Rac2 versus Rac1 functions in neutrophils and demonstrated that Rac2 controls its functions, at least in part, by distinct subcellular distributions of these GTPases (Tao et al, Blood 2002, Filippi et al, Nat Immunol 2004), highlighting one important mechanism controlling cellular functions. 

    Dr. Filippi's laboratory, in collaboration Dr. Yi Zheng, is now focused on determining the role of CDC42 and RhoA in neutrophil migration and in determining specifically the role of RhoA in hematopoietic stem cell migration and proliferation using gene targeted knock out mice for CDC42 and RhoA and their respective regulator CDC42GAP and 190RhoGAP. These studies will use in vitro and in vivo assays of cell migration as well as immunofluorescence microscopy to study cytoskeleton rearrangement associated with cell migration. 

    The long term goal of these studies is to identify new molecular targets of potential therapeutic importance.

    Visit the Filippi Lab.

    Education and Training

    PharmD: University of Rene Descartes, Paris, France, 1998.

    Residency: Hematopathology, University of Rene Descartes, Assistance public Hospital of Paris, Paris, France.

    Certification: Hematopathology, 2001.

    PhD: University of Denis Diderot, Paris, France, 2001.

    Publications

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    Grants

    Regulation of Neutrophil Migration and Polarity. National Institutes of Health. Mar 2010 - Mar 2015. #R01 HL 090676.
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    Fred Finkelman, MD

    is interested in the use of in vivo mouse models to study both basic immunology and disease pathogenesis. More specifically, he is trying to understand how cytokines and other immune mechanisms control intestinal worms infections; allergic, asthmatic, and anaphylactic diseases; as well as T cell memory.

    513-636-6656
    finkelfd@ucmail.uc.edu

    Fred Finkelman, MD

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-6656

    Email: finkelfd@ucmail.uc.edu

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    Specialties

    Rheumatology; cytokine control of immune-mediated disorders and host protection against parasites, cytokine regulation of allergic disorders, cytokine regulation of lymphopoiesis; regulation of cytokine responses and mechanisms of lymphocyte activation and tolerance; anaphylaxis; transfusion-related acute lung injury

    Publications

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    Grants

    IL-13 associated eosinophil lung responses. Co-principal Investigator. National Institutes of Health. Jul 2009 - Jun 2014.
    A photo of Matthew J. Flick.

    Matthew J. Flick, PhD

    is working to understand how hemostatic factors in the blood that are responsible for clotting also drive inflammation in the context of infection and diseases such as arthritis and fatty liver disease.

    513-636-6628
    matthew.flick@cchmc.org

    Matthew J. Flick, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-6628

    Email: matthew.flick@cchmc.org

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    Specialties

    Hemostatic factors and arthritis pathogenesis

    Biography

    Research Interests and Focus:

    1. Activation of the coagulation system, including the central coagulation protease thrombin, is a prominent feature of both human rheumatoid arthritis and experimental inflammatory arthritis. The long-term goal of Dr. Flick's research program is to determine how thrombin drives inflammatory joint disease. The proposed work will fill significant gaps in the understanding of the interplay between the thrombin- fibrinogen axis and arthritic disease, and may provide the proof-of-principle for the use of novel "customized" thrombin mutants with selected substrate specificity to treat arthritis.

    2. The pervasive gram-positive bacteria Staphylococcus aureus is a common pathogen that is the causative agent for a wide spectrum of diseases including skin infections, pneumonia, bacteremia, toxic-shock syndrome and sepsis. Notably, this pathogen has evolved and maintained a number of proteins that directly engage the host hemostatic system, including factors that directly interact with the host coagulation factor fibrinogen. The long-term goal of his research program is to understand how bacterial derived proteins interact with host factors to promote bacterial virulence in the context of blood-born infections. This work will provide novel insight into the molecular pathways by which S. aureus invades and disseminates within host tissues and may shed light into novel strategies for eliminating this potentially devastating infectious agent.

    3. Obesity is a worldwide epidemic linked to numerous disease sequelae, including non-alcoholic fatty liver disease (NAFLD). This spectrum disorder can progress from the simple accumulation of triglycerides within hepatocytes (i.e., steatosis), to inflammatory steatohepatitis, to organ failure secondary to irreversible liver fibrosis and cirrhosis. Dysregulation of the coagulation system has been documented in both patients with fatty liver disease and animal models of NAFLD, but any contribution to disease progression has remained largely undefined. Using a murine model of high fat diet (HFD)-induced NAFLD, they are testing the hypothesis that thrombin activity and fibrin deposition drive local inflammatory events promoting the progression of steatosis and steatohepatitis. Comparative studies of wild-type mice with genetically imposed deficiencies or functional alterations in prothrombin, fibrinogen and other associated coagulation factor components suggests that the thrombin-fibrinogen axis influences NAFLD pathogenesis by controlling local inflammatory processes that drive steatosis and by an unanticipated and unknown mechanism tying fibrin(ogen) to HFD-induced weight gain/obesity. Their research has far-reaching implications not only for the treatment and prevention of fatty liver disease, but also for all the downstream sequelae of obesity and even the development of diet-mediated weight gain itself.

    Education and Training

    BS: Xavier University, Cincinnati, OH.

    PhD: Purdue University, West Lafayette, IN.

    Post-doctoral Fellow: Cincinnati Children’s Hospital and Medical Center, Division of Developmental Biology, Cincinnati, OH.

    Publications

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    Grants

    Mechanisms linking the hemostatic protease thrombin to arthritic disease. Principal Investigator. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Jul 2009-Jun 2014. #R01 AR056990.

    Thrombin-mediated proteolysis in neuroinflammatory disease. Co-investigator. National Heart, Lung, and Blood Institute. Jul 2009-Jun 2014. #R01 HL096126.

    NIH, National Institute of Arthritis and Musculoskeletal and Skin Diseases Research. Director. Cincinnati Rheumatic Diseases Core Center. Aug 2011-Jun 2016. 2P30 AR47363. 

    Hemostatic factors and sickle cell disease. Co-investigator. NIH. Dec 2011-Nov 2016. R01 HLI12603.

    Analysis of Staphylococcus Host Interactions. Co-investigator. NIH. Sep 2010-Aug 2015. R01 AI020662.

    A photo of Lee Grimes.

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

    focuses his research on the genetic development of cancerous cells and inherited blood diseases. His lab utilizes the Growth factor independent-1 transcription factor as a molecular probe to dissect hematopoiesis and leukemia. Dr. Grimes serves as the director of the Cancer Pathology Program of the Divisions of Experimental Hematology and Pathology.
    Visit the Grimes Lab.

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

    H. Leighton (Lee) Grimes, PhD

    Director, Cancer Pathology Program of the Division of Experimental Hematology and the Division of Pathology

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

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-6089

    Fax: 513-636-5355

    Email: lee.grimes@cchmc.org

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    Specialties

    Transcriptional control of hematopoiesis and cancer.

    Visit the Grimes Lab.

    Biography

    Grimes Laboratory:

    The cloning and characterization of oncoproteins and tumor suppressors over the last 25 years has not only resulted in a greater understanding of the molecular mechanisms of transformation, but it has also provided a large set of therapeutic targets. Our lab is interested in the progression of a cell with a single genetic lesion to an invasive cancer with multiple genetic alterations. We focus on the Growth factor independence-1 (Gfi1) transcription factor, which is poorly oncogenic alone, but which potently collaborates with well known oncoproteins such as c-MYC. Gfi1 is the most frequently targeted gene in Moloney murine leukemia virus-induced tumors and induces tumor progression to cytokine-independent growth. In contrast, loss of Gfi1 in hematopoietic stem cells induces cell cycle progression and eventual bone marrow failure; implicating Gfi1 as a tumor suppressor in such cells. Gfi1 null mice have no mature neutrophils, and we have identified humans with Severe Congenital Neutropenia (SCN) and Non-Immune Chronic Idiopathic Neutropenia of Adults (NI-CINA) bearing mutations in Gfi1. Interestingly, such patients are at increased risk for the development of myelodysplastic syndromes and acute myeloid leukemia. We have recently generated the first mouse model of Severe Congenital Neutropenia through the expression of mutant Gfi1 proteins in primary murine hematopoietic cells. Moreover, we are utilizing mouse models of human cancer to assess the risk of Gfi1 mutant humans for the development of acute myeloid leukemia.

    Education and Training

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

    Postdoctoral Fellow: Fox Chase Cancer Center.

    Publications

    View PubMed Publications
    A photo of John Harley.

    John B. Harley, MD, PhD Director, CAGE

    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

    John B. Harley, MD, PhD

    Director, CAGE

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-803-3665

    Email: john.harley@cchmc.org

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    Publications

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    Grants

    Molecular & Immunologic Analysis of the Pathobiology of Human Anthrax. Co-Principal Investigator. National Institute of Allergy and Infectious Diseases. Sep 2009-Aug 2014. #AI062629-06.

    Genomics of Lupus. Principal Investigator. Aug 2009-Jul 2014. #1 P01 AI083194-01.
    A photo of Gurjit Khurana Hershey.

    Gurjit Khurana Hershey, MD, PhD Director, Division of Asthma Research

    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

    Gurjit Khurana Hershey, MD, PhD

    Director, Division of Asthma Research

    Co-Director, Office of Pediatric Clinical Fellowships

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-7054

    Fax: 513-636-1657

    Email: gurjit.hershey@cchmc.org

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    Specialties

    Clinical

    Asthma; allergic rhinitis; food allergy; urticaria

    Research

    Genetics of allergy and asthma; cytokines; signaling pathways

    Visit the Khurana Hershey Lab.

    Biography

    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. 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.

    Publications

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    A photo of David Hildeman.

    David A. Hildeman, PhD Director, Immunology Graduate Program

    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.

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

    David A. Hildeman, PhD

    Director, Immunology Graduate Program

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-3923

    Fax: 513-636-5355

    Email: david.hildeman@cchmc.org

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    Specialties

    Clinical Interests

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

    Research Interests

    Our lab is primarily interested in molecular factors that control the decision between tolerance and immunity within T lymphocytes. We use staphylococcal enterotoxins, recombinant vaccinia viruses, lymphocytic choriomeningitis virus and MHC tetrameric reagents as tools to study antigen -specific T cell responses. Our interest in 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. We are also interested in the manipulation and regulation of antigen-specific T cell responses via novel vaccine strategies to either induce tolerance or enhance immunity. Finally, we are interested in mechanisms underlying sex-based differences in T cell responses and how these differences relate to autoimmune disease.

    Education and Training

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

    Publications

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    A photo of Kasper Hoebe.

    Kasper Hoebe, PhD

    focuses on mechanistic analysis of pathways of innate immune activation and the mechanisms underlying NK cell and CD8+ T cell development and cytolytic effector function, using forward genetic approaches. His discovery of an “endogenous adjuvant” pathway mediated by NK cell killing has led to research aimed at exploiting the knowledge obtained on NK cell-driven adaptive immune responses for the generation of new, safer vaccine approaches.

    513-803-1056
    kasper.hoebe@cchmc.org

    Kasper Hoebe, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-803-1056

    Fax: 513-636-5355

    Email: kasper.hoebe@cchmc.org

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    Specialties

    Innate-adaptive connection; mechanisms underlying NK cell and CD8+ T cell development; cytolytic effector function; safer vaccine approaches

    Education and Training

    BS: Biology; Utrecht University, The Netherlands, 1994.

    PhD: Immunology/ Pharmacology; Utrecht University, The Netherlands, 2001.

    Publications

    View PubMed Publications
    A photo of Simon P. Hogan.

    Simon P. Hogan, PhD Director of Research, Division of Allergy and Immunology

    is studying allergies, food allergies, eosinophil biology & gastrointestinal inflammation.
    Visit the Hogan Lab.

    513-636-6620
    simon.hogan@cchmc.org

    Simon P. Hogan, PhD

    Director of Research, Division of Allergy and Immunology

    Director of Admissions, Immunology Graduate Program

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-6620

    Fax: 513-636-3310

    Email: simon.hogan@cchmc.org

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    Specialties

    Food allergies and anaphylaxis; inflammatory bowel diseases (IBD); innate immunity; gastrointestinal immunity and function; cystic fibrosis (CF)

    Visit the Hogan Lab.

    Education and Training

    BSC: Australian National University, Canberra, Australia, 1998.

    PhD: John Curtin School of Medical Research, Australian National University, Canberra, Australia, 1998.

    Publications

    View PubMed Publications

    Grants

    MiR-375 regulation of CFTR expression and Cl- secretory function. Principal Investigator. Cystic Fibrosis Foundation. Jul 2012-Jun 2014.

    Eosinophil:M2 Macrophage:CCL11 Axis in Experimental Colitis and Pediatric Corticosteroid Resistant UC. Principal Investigator.  National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (NIH/NIDDK). Apr 2012-Mar 2016.

    Epithelial Genes in Allergic Inflammation. Project 2 – Collaborating Investigator. National Institutes of Health/National Institute of Allergy and Infectious Diseases (NIH/NIAIDS). Sep 2006-Aug 2016.

    A photo of Margaret Hostetter.

    Margaret K. Hostetter, MD BK Rachford Professor and Chair, Department of Pediatrics

    studies the pathogenesis of bloodstream infections caused by the yeast Candida albicans. Her work has highlighted the role of C. albicans in biofilms, activation of human T cells, and evasion of innate immune mechanisms. Her clinical research is focused on the medical evaluation of internationally adopted children.

    513-636-4509
    margaret.hostetter@cchmc.org

    Margaret K. Hostetter, MD

    BK Rachford Professor and Chair, Department of Pediatrics

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-4509

    Email: margaret.hostetter@cchmc.org

    Show All

    Specialties

    Bacterial and fungal infections; medical evaluation of internationally adopted children

    Education and Training

    MD: Baylor College of Medicine.

    Residency: Boston Children’s Hospital.

    Training Fellowship: Boston Children’s Hospital.

    Board Certification: Pediatrics; Pediatric Infectious Diseases.
    A photo of Edith Janssen.

    Edith Janssen, PhD

    focuses on mechanistic analysis and translational exploitation of the processes in dendritic cells that balance pro- and anti-inflammatory immune responses to self after cell death. Dr. Janssen aims at harnessing dendritic cells to develop effective autologous cancer vaccines. Her recent discovery (with Dr. Jonathan Katz) that dysregulation of such cells suggests a potential role for therapeutic modulation of these cells in autoimmune disease.

    513-803-1055
    edith.janssen@cchmc.org

    Edith Janssen, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-803-1055

    Fax: 513-636-5355

    Email: edith.janssen@cchmc.org

    Show All

    Education and Training

    MS: Utrecht University, The Netherlands, 1995.

    PhD: Utrecht University, The Netherlands, 1999.

    Publications

    View PubMed Publications
    A photo of Michael Jordan.

    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.

    513-636-7287
    michael.jordan@cchmc.org

    Michael B. Jordan, MD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-7287

    Fax: 513-803-1969

    Email: michael.jordan@cchmc.org

    Show All

    Specialties

    Clinical Interests

    Histiocytic disorders: HLH and LCH

    Research Interests

    Better understanding histiocytic disorders and developing novel therapies for them; regulation of the immune response; immunotherapy of cancer

    Education and Training

    MD: UT Southwestern, Dallas, TX, 1993.

    Residency: Children's Hospital of Dallas, 1996.

    Fellowship: The Children's Hospital (Denver), 2002.

    Certification: American Board of Pediatrics, 1996; Sub-board of Pediatric Heme/Onc, 2002.

    Publications

    View PubMed Publications
    A photo of Theodosia A. Kalfa.

    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

    Theodosia A. Kalfa, MD, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-0989

    Fax: 513-636-3549

    Email: theodosia.kalfa@cchmc.org

    Show All

    Specialties

    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.

    Publications

    View PubMed Publications

    Grants

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

    Erythrocyte Cytoskeleton Disorders Diagnostic Core. Principal Investigator. CCTST PCS T1 Pilot. July 2013- June 2015.

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

    TCD with Transfusions Changing to Hydroxyurea. Co-investigator. NIH/Baylor. Aug 2009-Jul 2014. #R01HL095647.

    A photo of Jonathan Katz.

    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.

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

    Jonathan D. Katz, PhD

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-5306

    Fax: 513-636-5355

    Email: jonathan.katz@cchmc.org

    Show All

    Specialties

    Clinical Interests

    T cells; MHC, beta cell death; islet antigens

    Research Interests

    Immunology, autoimmunity, type 1 diabetes

    Biography

    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 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 similar to the T1D seen in human patients. The availability of the NOD strain has allowed us to take a modern, reductionist molecular and cellular immunology approach to understanding the mechanism(s) and genetics underlying T1D susceptibility and disease progression. His 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, Calif., 1984.

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

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

    Publications

    View PubMed Publications
    A photo of Ashish Kumar.

    Ashish R. Kumar, MD, PhD

    is a pediatric hematologist-oncologist who has a research program investigating the biology of leukemia caused by MLL-fusion genes. These leukemias are most common in infants and frequently fatal. The research in Dr. Kumar's lab is focused at identifying downstream targets of MLL-fusion proteins that could be exploited to develop novel therapies. Currently, the Kumar lab is investigating the role of MEIS1 in MLL-leukemia.
    Visit the Kumar Lab.

    513-803-1631
    ashish.kumar@cchmc.org

    Ashish R. Kumar, MD, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-803-1631

    Fax: 513-636-3549

    Email: ashish.kumar@cchmc.org

    Show All

    Specialties

    Clinical Interests

    Childhood cancer and blood disorders; immune deficiency

    Research Interests

    Leukemia biology; cancer biology

    Visit the Kumar Lab.

    Biography

    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. As a faculty of the Masonic Cancer Center, he was also part of the Genetic Mechanisms of Cancer research program. 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.

    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.

    Publications

    View PubMed Publications
    A photo of Ian Lewkowich.

    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.

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

    Ian P. Lewkowich, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-3999

    Email: ian.lewkowich@cchmc.org

    Show All

    Specialties

    Immunology; asthma

    Biography

    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.

    Publications

    View PubMed Publications

    Grants

    Mechanisms of steroid resistance in severe asthma. Principal Investigator. ATS Unrestricted Research Grant. Oct 2011 - Jul 2013.

    Synergistic Role of IL-17 and IL-13 in asthma susceptibility. Principal Investigator. Parker B Francis Fellowship. Jul 2010 - Jun 2013.
    A photo of Punam Malik, MD.

    Punam Malik, MD Marjory J. Johnson Chair of Gene and Cell Therapy

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

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

    Punam Malik, MD

    Marjory J. Johnson Chair of Gene and Cell Therapy

    Director, Comprehensive Sickle Cell Program

    Director, Translational Trials Development and Support Laboratory

    Program Leader, Hematology and Gene Therapy Program

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-1333

    Fax: 513-636-1330

    Email: punam.malik@cchmc.org

    Show All

    Education and Training

    MBBS: University of Delhi, New Delhi, India, 1985.

    MD: University of Delhi, New Delhi, India, 1989.

    MS: University of Maryland, Baltimore, MD, 1991.

    Fellowship: Children's Hospital Los Angeles, University of Southern California, 1995.

    Publications

    View PubMed Publications
    A photo of Alexander Miethke.

    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.

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

    Alexander G. Miethke, MD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-8948

    Email: alexander.miethke@cchmc.org

    Show All

    Specialties

    Clinical Interests

    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 Interests

    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

    Biography

    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. 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, 2009.

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

    Publications

    View PubMed Publications

    Grants

    Regulatory T cells and the pathogenesis of biliary atresia. Principal Investigator. American Liver Foundation. Jul 2009 - Jun 2012.

    Clinical center for cholestatic liver disease in children. Co-Investigator. National Institutes of Health. Jul 2009 - Jul 2014. #RFA-DK-08-005.
    A photo of Dr.Sean Moore.

    Sean R. Moore, MS, MD

    is interested in the vicious cycle of childhood diarrhea and malnutrition in developing countries, with a current focus on the mechanisms of a promising glutamine-based oral rehydration and nutrition therapy. Dr. Moore studies the signaling pathways by which alanyl-glutamine promotes gut homeostasis and also collaborates with colleagues on the epidemiology and impact of early childhood diarrhea and undernutrition in impoverished settings.

    513-636-4464
    sean.moore@cchmc.org

    Sean R. Moore, MS, MD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-4464

    Fax: 513-636-7805

    Email: sean.moore@cchmc.org

    Show All

    Specialties

    Clinical Interests

    General gastroenterology; inflammatory bowel diseases

    Research Interests

    Diarrheal diseases; glutamine; global health

    Biography

    The Gastroenterology, Hepatology and Nutrition laboratory is broadly interested in the reciprocal cycle of childhood diarrhea and malnutrition, with a current focus on the mechanisms of a promising glutamine-based oral rehydration and nutrition therapy. Using cellular and molecular techniques in both cell culture and an infant mouse model of undernutrition, we study the role of EGFR -- a key regulator of intestinal homeostasis -- in glutamine’s benefits for intestinal health.

    In addition, we participate in epidemiologic studies of early childhood diarrhea and undernutrition with colleagues at the Federal University of Ceará in Fortaleza, Brazil and the University of Virginia.

    Education and Training

    BA: Chemistry & Biology, Asbury College, Wilmore, KY.

    MS: Epidemiology, University of Virginia, Charlottesville, VA.

    MD: Johns Hopkins, Baltimore, MD, 2003.

    Residency: Vanderbilt University, Nashville, TN, 2006.

    Fellowship: Vanderbilt University, Nashville, TN 2009.

    Certification: Pediatrics, 2006.

    Publications

    View PubMed Publications
    A photo of Ardythe Morrow.

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

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

    Ardythe L. Morrow, PhD

    Director, Center for Interdisciplinary Research in Human Milk & Lactation

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-7584

    Fax: 513-636-7509

    Email: ardythe.morrow@cchmc.org

    Show All

    Specialties

    Human milk; child health and nutrition

    Biography

    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 the University of Cincinnati College of Medicine and Cincinnati Children's Hospital Medical Center, where 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 4 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, Texas.

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

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

    Publications

    View PubMed Publications
    A photo of Takahisa Nakamura.

    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.

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

    Takahisa Nakamura, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-4744

    Email: takahisa.nakamura@cchmc.org

    Show All

    Specialties

    RNA-related inflammation in obesity and metabolic diseases 

    Biography

    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 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

    Publications

    View PubMed Publications

    Grants

    Functional analysis of PKR, JNK, and RISC in metabolic inflammation and homeostasis. Principal Investigator. American Heart Association, Scientist Development Grant. Jan 2012 – Dec 2014.

    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 Joseph Qualls.

    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

    Joseph E. Qualls, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-636-9102

    Email: joseph.qualls@cchmc.org

    Show All

    Specialties

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

    Biography

    Dr. Qualls completed his undergraduate work in 2002, receiving his BA summa cum laude in biology from Thomas More College in Crestview Hills, Kentucky. 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, Tennessee, 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.

    Current research: Many groups have shown that T cell function is inhibited via byproducts of L-arginine metabolism or when extracellular L-arginine becomes limiting. In one project, the laboratory is focused on characterizing the in vivo function of L-arginine utilization by macrophages during mycobacterial infection, and how this affects anti-pathogen T cell function. In parallel, the laboratory is addressing the provocative role of L-arginine biosynthesis from L-citrulline during intracellular infection, and how this mechanism is regulated at the cellular level. While greatly unexplored, this pathway of amino acid recycling is vital as mice deficient in L-arginine biosynthesis, compared to normal mice, lack efficient control of both M. bovis BCG and 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.

    Publications

    View PubMed Publications

    Grants

    Consequences of amino acid limitation on immune function. Principle Investigator. Cincinnati Children’s TAPS Program, Trustee Award. Jan. 2013 – Dec. 2014.
    A photo of Nancy Ratner.

    Nancy Ratner, PhD Beatrice C. Lampkin Chair, Cancer Biology

    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

    Nancy Ratner, PhD

    Beatrice C. Lampkin Chair, Cancer Biology

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-9469

    Fax: 513-636-3549

    Email: nancy.ratner@cchmc.org

    Show All

    Specialties

    Clinical Interests

    Development of the nervous system; peripheral nerve tumor formation

    Research Interests

    Genetic mutations in tumor suppressor genes

    Visit the Ratner Lab.

    Biography

    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 as a potential therapeutic target 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.

    Education and Training

    PhD: Indiana University, 1982.

    BA: Brown University, 1975.

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

    Publications

    View PubMed Publications

    Grants

    Mitogenic Activities in Neurofibromatosis. Principle Investigator. Sept 2011-2016. NIH-R01 NS 28840-20.
    A photo of Marc Rothenberg.

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

    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. Lab has identified and characterized several critical pathways that regulate allergic responses. 

    Visit the Rothenberg Lab web site

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

    Marc E. Rothenberg, MD, PhD

    Director, Division of Allergy and Immunology

    Director, Cincinnati Center for Eosinophilic Disorders

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-803-0257

    Fax: 513-636-3310

    Email: marc.rothenberg@cchmc.org

    Show All

    Specialties

    Clinical Interests

    Eosinophilia; eosinophilic disorders; asthma; allergy; food allergy

    Research Interests

    Eosinophils; chemokines

    Visit the Rothenberg Lab.

    Biography

    Dr. Rothenberg is director of the Division of Allergy/Immunology at Cincinnati Children's Hospital Medical Center and tenured professor of pediatrics at Cincinnati Children’s and 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 web site

    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.

    Publications

    Grants

    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.

    Immunobiology of Peanut Allergy and It’s Treatment. Co-Investigator. National Institutes of Health. Jul 2010–Jun 2015. U19 AI066738.

    Regulation of Gastrointestinal Eosinophils. Principal Investigator. National Institutes of Health. Dec 2009–Nov 2014. R37 AI045898.

    Cincinnati Center for Clinical and Translational Science and Training. Co-Program Director. National Institutes of Health. Apr 2009–Mar 2015. KL2 TR000078.

    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.

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    Nancy M. Sawtell, PhD

    leads studies of herpes simplex virus and has identified VP16, the first gene essential for triggering the virus’s emergence from its latent state in the human nervous system. Reactivation of the virus in the brains of older mice carrying the human APOE 4 gene to leads to lesions that resemble Alzheimer’s.
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    513-636-7880
    nancy.sawtell@cchmc.org

    Nancy M. Sawtell, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-7880

    Fax: 513-636-7655

    Email: nancy.sawtell@cchmc.org

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    Specialties

    Molecular mechanisms of herpes virus latency and reactivation; viral persistence; pathogenesis; animal models of disease

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    Education and Training

    BA: Chemistry, Case Western Reserve University, 1975.

    PhD: Pathology and Immunology, University of Cincinnati Medical College, Cincinnati, OH, 1986.

    Publications

    View PubMed Publications
    A photo of Daniel Starczynowski.

    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

    Daniel T. Starczynowski, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-803-5317

    Email: daniel.starczynowski@cchmc.org

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    Specialties

    Visit the Starczynowski Lab.

    Biography

    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 is continuing to investigate the molecular and cellular basis of MDS. The current objective of his research program is to understand the contribution of MDS-associated miRNAs and their targeted genes to the pathogenesis of MDS and progression to AML. He hopes that understanding some of the molecular causes of MDS will enhance our insight into the biology of MDS, and provide novel targeted therapies.

    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.

    Publications

    View PubMed Publications

    Grants

    Regulation and Function of TIFAB in Myelodysplastic Syndrome. Department of Defense. Jun 2011 - May 2014. #W81XWH1110468.
    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.
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    513-636-3899
    susan.thompson@cchmc.org

    Susan Thompson, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-3899

    Fax: 513-636-3328

    Email: susan.thompson@cchmc.org

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    Specialties

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

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    Biography

    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.

    Publications

    View PubMed Publications
    A photo of Stephen Waggoner.

    Stephen N. Waggoner, PhD

    is a viral immunologist whose lab studies immune regulatory mechanisms that control pathogenesis of disease. We use viruses and bacteria to probe immune functions associated with disease in mice. Our 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

    Stephen N. Waggoner, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-803-4607

    Email: stephen.waggoner@cchmc.org

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    Specialties

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

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    Biography

    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. 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.

    Publications

    View PubMed Publications

    Grants

    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 Yui-Hsi Wang.

    Yui-Hsi Wang, PhD

    investigates the mechanisms that govern the plasticity of tissue resident TH2 memory / effector cells in the airway and gut. Particularly interested in understanding how inflammatory mediators, such as IL-1b, IL-33 and IL-25, regulate the development of IL-17-producing TH2 or IL-9-producing TH2 cells during airway or gastrointestinal allergic inflammation, respectively. 

    513-803-2193
    yui_hsi.wang@cchmc.org

    Yui-Hsi Wang, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-803-2193

    Fax: 513-636-3310

    Email: yui_hsi.wang@cchmc.org

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    Specialties

    Asthma; food allergy; T cell biology

    Education and Training

    PhD: University of Alabama, Birmingham, AL, 2001.

    Publications

    View PubMed Publications

    Grants

    The roles of IL-17-producing TH2 memory/effector cells in allergic asthma. Principal Investigator. American Lung Association. July 2010 - June 2012. #AI-169584-N.

    Regulation and maintenance of TH2 memory/effector cells. Principal Investigator. National Institutes of Health. May 2010- April 2015. #R01AI090129-01.

    A photo of Sing Sing Way.

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

    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

    Sing Sing Way, MD, PhD

    Pauline and Lawson Reed Chair, Division of Infectious Diseases

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-7603

    Email: singsing.way@cchmc.org

    Show All

    Specialties

    Infectious diseases; prenatal infection; immunology

    Biography

    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.

    Publications

    View PubMed Publications

    Grants

    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. Principle Investigator. National Institute of Allergy and Infectious Diseases (NIAID). 2012-2017. R01-AI100934.

    Regulatory T cells dictate the immunity during persistent Salmonella infection. Principle Investigator. National Institute of Allergy and Infectious Diseases (NIAID). 2010-2015. R01-AI087830.

    A photo of Timothy Weaver.

    Timothy E. Weaver, MS, PhD Co-Director, Division of Pulmonary Biology

    focuses on the identification of cytoprotective pathways that mediate adaptation to genetic and environmental stresses in the pulmonary epithelium. These molecular pathways play a critical role in preventing or slowing the progression of chronic lung disease and may provide novel targets for therapeutic intervention.
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    513-636-7223
    tim.weaver@cchmc.org

    Timothy E. Weaver, MS, PhD

    Co-Director, Division of Pulmonary Biology

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-7223

    Fax: 513-636-7868

    Email: tim.weaver@cchmc.org

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    Specialties

    Research

    Lung development; chaperone biology and diseases of protein misfolding; pulmonary fibrosis; asthma; respiratory distress syndrome; acute and chronic lung disease

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    Biography

    Dr. Weaver has a long-standing interest in lung development and disease. His early work with Dr. Whitsett uncovered the function of surfactant proteins SP-B and SP-C, a discovery that has profoundly influenced the treatment of respiratory distress syndrome and survival of pre-term infants worldwide. His current research is focused to the molecular pathways (ER stress and autophagy) that link mutations in the SFTPC gene (encoding surfactant protein C) to development of interstitial lung disease (ILD) in both children and adults. His work has been continuously funded by the National Institutes of Health since 1986, including a MERIT (R37) award from the National Heart, Lung and Blood Institute (2001-2011).

    Dr. Weaver has trained 14 graduate students in the past 15 years and is the past director of the Molecular and Developmental Biology Graduate Program. During the same period of time he has trained 11 postdoctoral fellows, eight of whom are current faculty members at institutions in the US, Germany, France, Japan and UK.

    Education and Training

    BS: Biology, Bob Jones University, Greenville, South Carolina, 1975.

    MS: Embryology, Hahnemann Medical College, Philadelphia, Pennsylvania, 1979.

    PhD:
    Developmental Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio, 1983.

    Postdoc: Molecular Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio, 1986.

    Publications

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    Grants

    Role of Autophagy in Pathogenesis of Interstitial Lung Disease. Principal Investigator. National Institutes of Health. Jul 2011 - Jun 2015. R01-HL103923.

    Stard7, A Novel Inhibitor Of Allergic Lung Disease. Principal Investigator. National Institutes of Health. Dec 2013 - Nov 2017. R01-HL122130.

    A photo of Matthew Weirauch.

    Matthew T. Weirauch, PhD

    is a computational biologist.  His lab is interested in understanding the mechanisms of gene transcriptional regulation.  Current projects focus on the characterization of transcription factor binding specificities, and the development of methods for modeling their interactions with DNA, both in vitro and in vivo.  His lab also applies insights from basic research on transcription factor-DNA interactions to the study of the mechanisms underlying complex diseases, with particular emphasis on lupus.

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

    Matthew T. Weirauch, PhD

    Academic Information

    Assistant Professor, UC Department of Pediatrics

    Phone: 513-803-9078

    Email: matthew.weirauch@cchmc.org

    Show All

    Specialties

    Transcription factors; transcriptional regulation; functional genomics; genome analysis; network-based algorithms; bioinformatics

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    Biography

    The staggering diversity of life on our planet stems from the elegant system encoded in our genomes.   A major finding of the genomic era is that a substantial proportion of the wide range of biological form and function is likely explained by differences in gene regulation (the processes governing how and when genes are utilized), as opposed to differences in the genes themselves.  An important component of gene regulation is the binding of transcription factors (TFs) to genomic DNA.  A typical metazoan genome contains thousands of TFs, and knowledge of their sequence binding preferences is crucial to our understanding of the “regulatory code” governing health and disease. 

    Two major obstacles stand in our way before we can even begin to accurately model gene regulation.  First, we must gain a thorough knowledge of the sequence binding preferences of TFs.  Of an estimated 165,000 TFs present in the approximately 300 sequenced eukaryotic organisms, sequence preferences are currently known for only ~2,000 (~1%).  In collaboration with Tim Hughes at the University of Toronto, I have developed a joint experimental and computational approach to determine or predict binding preferences for > 55,000 eukaryotic TFs (>30%), representing an order of magnitude improvement over our current knowledge.  Second, there is an ongoing controversy surrounding the optimal way to represent TF binding preferences, and how to accurately model them to predict binding to genomic sequences.  To address this issue, I have recently led the largest evaluation of computational TF binding models to date, involving 20 methods developed by researchers from around the world.  Together, these two studies will provide the groundwork for the future development of models of gene regulation in both normal and disease states.

    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.

    Publications

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    Grants

    Lupus Association with Signal Transducer and Activator of Transcription 4. Investigator. US Department of Veterans Affairs. 2012.
    A photo of Susanne Wells.

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

    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

    Susanne Wells, PhD

    Director, Epithelial Carcinogenesis and Stem Cell Program

    Director, Postdoctoral Office

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-5986

    Fax: 513-636-3549

    Email: susanne.wells@cchmc.org

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    Specialties

    Squamous cell carcinoma; mechanisms by which the HPV oncogenes subvert the host cell machinery to promote abnormal cell growth and cancer; role of specific cellular HPV targets in viral replication and cellular transformation

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    Biography

    Susanne Wells graduated from the University of Konstanz, Germany, with a degree in Biology. She completed her PhD in Molecular Biology 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 human papillomavirus infection and associated carcinogenesis.

    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.

    Publications

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