ABSTRACT
Type 1 diabetes (T1D) is an autoimmune disease thought to result from the activation of T lymphocytes specific for autoantigens in insulin-producing pancreatic beta cells. The T cell response leads to decreasing endogenous insulin production which becomes clinically manifest when the remaining beta cell mass can no longer produce sufficient insulin to maintain glucose homeostasis. This immunopathologic basis of T1D is supported by several complementary lines of evidence including the following: The presence of circulating antibodies to beta cell antigens that predict disease
development (1). Genome-wide association studies have identified 10 genetic loci most strongly
associated with T1D susceptibility, six of which either influence immune function (MHC, CTLA4, CD25, PTPN2, MDA5) or the insulin-specific T-cell repertoire (insulin VNTR) (2).
