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

    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

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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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    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.

    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, 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
    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

    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

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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 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

    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 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

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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.

    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. 

    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

    View PubMed Publications
    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

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-3923

    Fax: 513-636-5355

    Email: david.hildeman@cchmc.org

    Show All

    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

    Show All

    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

    Show All

    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.

    Interleukin-9 in Experimental Intestinal Anaphylaxis. Principal Investigator. National Institutes of Health/ National Institute of Allergy and Infectious Diseases/ National Institute of Diabetes and Digestive and Kidney Diseases (NIH/NIAIDS/NIDDK). Dec 2007-Nov 2013.

    A photo of Margaret Hostetter.

    Margaret K. Hostetter, MD Director, Infectious Diseases

    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

    Director, Infectious Diseases

    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.
    janssen-edith-thumbnail

    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, MD.

    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

    Grants

    Hybrid Immunotherapy for Hemophagocytic Lymphohistiocytosis. Principal Investigator. Histiocytosis Association of America. Jan 2011 - Dec 2011.
    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, PhD.

    Jonathan D. Katz, PhD

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

    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, MD, PhD.

    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

    Assistant 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

    Grants

    Molecular Pathogenesis of MLL-Fusion Gene Leukemia. View PubMed Publications. Principal Investigator. National Institute of Health. Jul 2007 - Jun 2012.
    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 Director, Comprehensive Sickle Cell Program

    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

    Director, Comprehensive Sickle Cell Program

    Director, Translational Trials Development and Support Laboratory

    Program Leader, Molecular and Gene Therapy Program

    Academic Information

    Associate 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 appo