Our primary research interest is to understand the genetic basis for immunological tolerance to endogenous proteins. Defects in these mechanisms lead to many debilitating autoimmune diseases, of which type 1 diabetes (T1D) is one of the most serious. In both humans and NOD mice, T1D results when insulin-producing pancreatic ß-cells are destroyed by autoreactive T-cell responses. Thus, insights into the genetic mechanisms responsible for the normal maintenance of immunological tolerance can be gained by identifying the pathogenic basis of T1D in NOD mice.
