Molecular Immunology

Jonathan D. Katz, PhD

Appointment

Associate Professor of Pediatrics

Email

jonathan.katz@cchmc.org

Phone

513-636-5306

Fax

513-636-5355

Bio

Dr. Katz's laboratory 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.

Credentials

BS: Microbiology, University of California, Los Angeles, Calif., 1984.

PhD: Microbiology and Immunology, University of California, Los Angeles, Calif., 1990.

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

Awards and Honors

Recipient, Career Development Award, American Diabetes Association (ADA), 1996-1998.

Research

Immunology, Autoimmunity, Type 1 Diabetes

Research Grants and Contracts

2002-2007 Principal Investigator, USPHS R01 DK62274. Using genomics to understand autoimmune diabetes. $950,000 total direct

2006-2008 Principal Investigator, USPHS R21 DK75769. The Insulitis Reporter Mouse. $250,000 total direct

2006-2009 Principal Investigator, JDRF 1-2006-744. Pulling back the covers on insulitis. $495,000 total direct

Publications, Most Recent

View Jonathan Katz's publications as listed by PubMed.

Hamilton-Williams, E.E., X. Martinez, J. Clark, S. Howlett, K.M. Hunter, D.B. Rainbow, L. Wen, M.J. Shlomchik, J.D. Katz, G.F. Beilhack, L.S. Wicker and L.A. Sherman. 2009. Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice. J. Immunol. 183:1533-1541.
Saxena, V., J.K. Ondr, A.F. Magnusen, D.H. Munn and J.D. Katz. 2007. The countervailing actions of myeloid and plasmacytoid dendritic cells control autoimmune diabetes in the nonobese diabetic mouse. J. Immunol. 179:5041-5053.
Cain, J.A., J.A. Smith, J.K. Ondr, B. Wang and J.D. Katz. 2006. NKT cells and IFN-gamma establish the regulatory environment for the control of diabetogenic T cells in the nonobese diabetic mouse. J. Immunol. 176:1645-1654.
Vukkadapu, S.S., J.M. Belli, K. Ishii, A.G. Jegga, J.J. Hutton, B.J. Aronow and J.D. Katz. 2005. Dynamic interaction between T cell-mediated beta-cell damage and beta-cell repair in the run up to autoimmune diabetes of the NOD mouse. Physiol. Genomics 21:201-211.
Suri, A., J. Shimizu, J.D. Katz, S. Sakaguchi, E.R. Unanue and O. Kanagawa. 2004. Regulation of autoimmune diabetes by non-islet-specific T cells - a role for the glucocorticoid-induced TNF receptor. Eur. J. Immunol. 34:447-454.
Hutton, J.J., A.G. Jegga, S. Kong, A. Gupta, C. Ebert, S. Williams, J.D. Katz and B.J. Aronow. 2004. Microarray and comparative genomics-based identification of genes and gene regulatory regions of the mouse immune system. BMC Genomics 5:82.
Pakala, S.V., M. Chivetta, C.B. Kelly and J.D. Katz. 1999. In autoimmune diabetes the transition from benign to pernicious insulitis requires an islet cell response to tumor necrosis factor alpha. J. Exp. Med. 189:1053-1062.
Suri, A. and J.D. Katz. 1999. Dissecting the role of CD4+ T cells in autoimmune diabetes through the use of TCR transgenic mice. Immunol. Rev. 169:55-65.
Kanagawa, O., B.A. Vaupel, G. Xu, E.R. Unanue and J.D. Katz. 1998. Thymic positive selection and peripheral activation of islet antigen-specific T cells: separation of two diabetogenic steps by an I-A(g7) class II MHC beta-chain mutant. J. Immunol. 161:4489-4492.
Kurrer, M.O., S.V. Pakala, H.L. Hanson and J.D. Katz. 1997. Beta cell apoptosis in T cell-mediated autoimmune diabetes. Proc. Natl. Acad. Sci. U.S.A. 94:213-218.
Pakala, S.V., M.O. Kurrer and J.D. Katz. 1997. T helper 2 (Th2) T cells induce acute pancreatitis and diabetes in immune-compromised nonobese diabetic (NOD) mice. J. Exp. Med. 186:299-306.

Professional Organization Memberships

American Association of Immunologists

Juvenile Diabetes Foundation

American Diabetes Association

Immunology of Diabetes Society

American Association for the Advancement of Science

Special Interests

T cells; MHC, Beta cell death; Islet antigens.

Reviwer/Editor Responsibilities

Juvenile Diabetes Research Foundation International, Medical Science Research Committee (Immunology)
Ad hoc, National Institute of Health (NIDDK and NIAID), Special Emphasis Panels
Ad hoc, Wellcome Trust, London, England
Ad Hoc, NIH-CSR, Immunological Sciences (IMS) Study Section
Member, Howard Hughes Medical Institute, Pre-doctoral Fellowship Review Panel
Member, Hypersensitivity, Inflammation and Allergy (HAI) Study Section
Associate Editor, Journal of Immunology
Member, Editorial Board, Diabetes