Immunobiology

  • Research Faculty

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    Division Head

    A photo of Harinder Singh.

    Harinder Singh, PhD Director, Division of Immunobiology

    513-636-7641
    harinder.singh@cchmc.org

    Harinder Singh, PhD

    Director, Division of Immunobiology

    Academic Information

    Professor, UC Department of Pediatrics

    Phone: 513-636-7641

    Email: harinder.singh@cchmc.org

    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 Claire Chougnet.

    Claire A. Chougnet, PhD

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

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

    Claire A. Chougnet, PhD

    Academic Information

    Associate Professor, UC Department of Pediatrics

    Phone: 513-636-8847

    Fax: 513-636-4278

    Email: claire.chougnet@cchmc.org

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    Specialties

    Clinical Interests

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

    Research Interests

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

    Education and Training

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

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

    PhD: Université Paris V, 1991.

    Publications

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    A photo of 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.
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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 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

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    A photo of David Hildeman.

    David A. Hildeman, PhD Director, Immunology Graduate Program

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

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

    David A. Hildeman, PhD

    Director, Immunology Graduate Program

    Academic Information

    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

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    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; Utrecht University, The Netherlands, 1994.

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

    Publications

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    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

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    Education and Training

    MS: Utrecht University, The Netherlands, 1995.

    PhD: Utrecht University, The Netherlands, 1999.

    Publications

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    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

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    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

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    Grants

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

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    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

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    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

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    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

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    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 Yrina Rochman.

    Yrina Rochman, PhD

    is focused on elucidating molecular mechanisms of immunological responses. Particularly, on the role of cytokines in the adaptive immune response and T cell differentiation.


    yrina.rochman@cchmc.org

    Yrina Rochman, PhD

    Academic Information

    Instructor, UC Department of Pediatrics

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    Specialties

    Research

    Immunology

    Biography

    Yrina earned her PhD from the Hebrew University of Jerusalem. She completed her post-doctoral training in molecular immunology at National Institutes of Health in the laboratory of Dr. Warren Leonard, where she published several papers and reviews in high profile peer-reviewed journals. She is a recipient of the Lenfant Biomedical Award from NHLBI, NIH for outstanding research. Her research is focused on elucidating molecular mechanisms of immunological responses.

    Education and Training

    PhD: Hebrew University of Jerusalem, Israel, 2005.

    Post-Doc Fellowship: NHLBI/National Institutes of Health, Bethesda, MD, 2005-2011.

    Research Associate: Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2012-2013.

    Research Instructor: Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2013-present.

    Publications

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