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.
T cells; MHC, beta cell death; islet antigens
Immunology; autoimmunity; type 1 diabetes
Professor, UC Department of Pediatrics
Molecular Immunology, Endocrinology, Immunobiology