A photo of Jonathan Katz.

Professor, UC Department of Pediatrics

513-636-5306

513-636-5355

Biography & Affiliation

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 is 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 similarity to the T1D seen in human patients. The availability of the NOD strain has allowed the lab to take a modern, reductionist molecular and cellular immunology approach to understanding the mechanism(s) and genetics underlying T1D susceptibility and disease progression. Dr. Katz's 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.

Clinical Interests

T cells; MHC, beta cell death; islet antigens

Research Interests

Immunology; autoimmunity; type 1 diabetes

Academic Affiliation

Professor, UC Department of Pediatrics

Departments

Molecular Immunology, Endocrinology, Immunobiology

Education

BS: University of California, Los Angeles, CA, 1984.

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

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

Publications

Extending Remission and Reversing New-Onset Type 1 Diabetes by Targeted Ablation of Autoreactive T Cells. Carroll, KR; Elfers, EE; Stevens, JJ; McNally, JP; Hildeman, DA; Jordan, MB; Katz, JD. Diabetes. 2018; 67:2319-2328.

Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases. McNally, JP; Millen, SH; Chaturvedi, V; Lakes, N; Terrell, CE; Elfers, EE; Carroll, KR; Hogan, SP; Andreassen, PR; Kanter, J; et al. Proceedings of the National Academy of Sciences of USA. 2017; 114:E4782-E4791.

Dying to protect: cell death and the control of T-cell homeostasis. Li, K; Shanmuganad, S; Carroll, K; Katz, JD; Jordan, MB; Hildeman, DA. Immunological Reviews. 2017; 277:21-43.

Reversal of New-Onset Type 1 Diabetes With an Agonistic TLR4/MD-2 Monoclonal Antibody. Bednar, KJ; Tsukamoto, H; Kachapati, K; Ohta, S; Wu, Y; Katz, JD; Ascherman, DP; Ridgway, WM. Diabetes. 2015; 64:3614-3626.