Immunobiology 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 Assistant Professor, Genetics and Allergy & Immunology

    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

    Assistant Professor, Genetics and Allergy & Immunology

    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 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

    Grants

    Role of chromatin and gene poising in T cell differentiation and activation. Principal Investigator. National Institutes of Health. 2009 - 2004. #1K22HL098691-01.
    A photo of Jorge Bezerra.

    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

    Jorge A. Bezerra, MD

    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

    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. 

    Grants

    The plasminogen system and liver repair. Principal Investigator. National Institutes of Health. 2000 - 2011. #R01 DK 55710.
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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, Division of Pediatric 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

    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.

    Rac GTPase Inhibition in Chronic Myelogenous Leukemia. Principal Investigator. National Institutes of Health. Apr 2009 – Feb 2014. #R01 HL 087159.

    Improving Hematopoietic Stem Cell Mobilization by the EGFR inhibitor Erlotinib. Co-Principal Investigator with Hartmut Geiger. NIH/NHLBI. Feb 2011 – Jan 2013. #R43HL108403-01.

    Connexin-43 in Bone Marrow Failure After Cancer-Related Chemotherapy. Principal Investigator. Heimlich Institute. Apr 2010 – Mar 2013.

    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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    Grants

    Homeostasis and function of regulatory T cells in aging. National Institutes of Health. Sep 2009 - Sep 2011. #R01 AG033057 ARRA.

    Dysfunction in biliary atresia. National Institutes of Health. Aug 2003 - Dec 2011. #R01 DK 065008.

    Late Preterm Birth, Ureaplasma Species and Childhood Lung Disease. National Institutes of Health. Aug 2009 - Jul 2013. #R01 HL097064-01.

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    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

    George Deepe, MD

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-558-4704

    Email: george.deepe@uc.edu

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    Specialties

    Host response to fungi

    Education and Training

    AB: Kenyon College, English and Biology, 1971.

    MD: University of Cincinnati College of Medicine, 1976.

    Publications

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    Grants

    GM-CSF Regulation of Zinc in Histoplasmosis. Principal Investigator. National Institutes of Health. Feb 2011 - Feb 2013.

    Immunopathogenesis in Histoplasmosis. Principal Investigator. National Institutes of Health. Jun 2008 - May 2013.

    Molecular and Cellular Determinants of Immunity in Histoplasmosis. Principal Investigator. Veterans Affairs. Apr 2010 - Mar 2014.

    Chemokine-Cytokine Nexus in Fungal Immunity. Principal Investigator. National Institutes of Health. Feb 2010 - Jan 2015.

    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

    Hemostatic factors as determinants of bacterial virulence and host defense. Principal Investigator. National Heart, Lung and Blood Institute. Sep 2006 – Aug 2011. #R01 HL085357.

    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

    Defining the mechanisms underlying inflammation-driven preterm birth. Principal Investigator. Cincinnati Children’s Hospital Medical Center, Perinatal Institute Pilot and Feasibility Application. Jul 2011 - Jun 2013.

    IL-17 axis in pathogenesis of NASH. Principal Investigator. Cincinnati Children’s Hospital Medical Center, Trustee Grant. Jan 2012 - Dec 2013.

    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, PhD.

    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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    Specialties

    I am 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 my post-doc in the laboratory of Dr David Williams, we 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, we 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, we 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.

    My 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 Hematopoietic Stem Cell Self Renewal. Principal Investigator. National Institutes of Health. Aug 2010 - Aug 2012. #R21 HL 104458.

    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
    ffinkelman@pol.net

    Fred Finkelman, MD

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-6656

    Email: ffinkelman@pol.net

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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

    Pathogenesis and prevention of anaphylaxis induced by ingested antigens. Veterans Association. National Institutes of Health. Apr 2008 - Mar 2012.

    IgG isotype regulation of antibody-mediated disorders. Principal Investigator. National Institutes of Health. Oc 2009 - Aug 2012.

    Alternative macrophage activation limits immunopathology. Co-principal Investigator. National Institutes of Health. Dec 2007 - Nov 2012.

    Multidisciplinary clinical research center in Cincinnati Project 2 - Improved understanding of the biology and use of TNF inhibition in JIA. Co-principal Investigator. National Institutes of Health. Apr 2008 - Mar 2013.

    Regulation of CD8+ T cell homeostasis by IL-4. Principal Investigator. National Institutes of Health. Oct 2008 - Dec 2013.

    IL-13 associated eosinophil lung responses. Co-principal Investigator. National Institutes of Health. Jul 2009 - Jun 2014.

    A photo of Matthew Flick, PhD.

    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

    View PubMed Publications

    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.

    Coagulation factors and the pathogenesis of non-alcoholic fatty liver disease. Principle Investigator. Cincinnati Children’s Hospital Digestive Health Center (DHC) Pilot and Feasibility Grant. Jun 2012 - May 2013. P30 DK078392.

    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 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 Grimes, PhD

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

    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 Dr. John Harley.

    John B. Harley, MD, PhD Director, Rheumatology

    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, Rheumatology

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-803-3665

    Email: john.harley@cchmc.org

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    Publications

    View PubMed Publications

    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.

    Oklahoma Autoimmunity Center of Excellence Project 2. Co-investigator. National Institute of Allergy and Infectious Diseases. May 2009 - Apr 2014. #1 U19 AI082714-01.

    Genome-Wide Association Study in African-Americans with Systemic Lupus Erythematosus. Principal Investigator. Department of Defense. Sep 2010- Aug 2013. #PR094002.

    Genomics of Lupus Associations in the Hispanic 12q24 Linkage. Principal Investigator. National Institutes of Health. Jun 2008 - Mar 2013. #5 P01 AR049084-07.

    Lupus Association with Signal Transducer and Activator of Transcription 4. Principal Investigator. US Department of Veterans Affairs. Apr 2008 - Mar 2012.

    Genetic Linkage in Lupus. Principal Investigator. National Institute of Allergy and Infectious Diseases. Feb 2010 - Jan 2012. #3 R37 AI024717-21S1.

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    Andrew Herr, PhD

    studies protein-protein interactions involved in bacterial pathogenesis, immune regulation, and thrombosis. His laboratory uses the complementary techniques of biophysical chemistry and X-ray crystallography to understand how cell-surface proteins recognize their ligands and mediate their biological function.
    Visit the Herr lab.

    513-558-5312

    Andrew Herr, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-558-5312

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    Specialties

    Biophysical and crystallographic studies of cellular adhesion and receptor signaling

    Education and Training

    BA: Biomedical Chemistry, Oral Roberts University, Tulsa, OK.

    PhD: Molecular Biophysics , Washington University, St. Louis, MO.

    Fellowship: California Institute of Technology, Pasadena, CA.

    Publications

    View PubMed Publications
    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. 

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

    Gurjit Khurana Hershey, MD, PhD

    Director, Division of Asthma Research

    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 Interests

    Asthma; allergic rhinitis; food allergy; urticaria

    Research Interests

    Genetics of allergy and asthma; cytokines; signaling pathways

    Biography

    Khurana Gurjit 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 Associate Director of the Physician 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. She is the Principal Investigator of an NIH-funded Asthma and Allergic Diseases Cooperative Research Center (AADCRC) and serves on the AADCRC steering committee. This Center is focused on characterizing epithelial genes in allergic diseases, and delineating the mechanisms by which they contribute to the allergic response. She is also a co-investigator of the NIEHS-funded Cincinnati Childhood Asthma and Air Pollution Study, a birth cohort study designed to elucidate gene:environment interactions relevant to the development of allergic disease in early life. In addition to her research contributions, she is an outstanding clinician and teacher/mentor. Several of her trainees now hold academic faculty positions.

    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 and is the Chair of the Genetics, Molecular Biology, and Epidemiology Committee. She serves on the Editorial Board of the Journal of Allergy and Clinical Immunology and on a regular NIH study section. 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.

    MD, PhD: 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.

    Publications

    View PubMed Publications
    A photo of David Hildeman.

    David A. Hildeman, PhD Director, Immunobiology 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 Immunobiology Graduate Program.

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

    David A. Hildeman, PhD

    Director, Immunobiology Graduate Program

    Academic Information

    Associate 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

    View PubMed Publications

    Grants

    Regulation of Apoptosis in Activated Primary T Cells. Principal Investigator. National Institute of Allergy and Infectious Diseases. Dec 2008 – Nov 2013. #R01 AI057753. 

    Homeostasis and function of regulatory T cells in aging. Co-Principal Investigator. National Institute on Aging. Sep 2009 - Aug 2011.  #RO1 AG3054748.
    A photo of Kasper Hoebe, PhD.

    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; Ultrecht University, The Netherlands, 1994.

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

    Publications

    View PubMed Publications
    A photo of Simon P. Hogan.

    Simon P. Hogan, PhD Director of Admissions, Immunobiology Graduate Program

    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 Admissions, Immunobiology Graduate Program

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-6620

    Fax: 513-636-3310

    Email: simon.hogan@cchmc.org

    Show All

    Specialties

    Allergies; food allergies; eosinophil biology; gastrointestinal inflammation

    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

    Interleukin-9 in Experimental Intestinal Anaphylaxis. Principal Investigator. National Institute of Health. Dec 2007 - Nov 2012. #NIH RO1 A1073553-01.
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