Abstract
Classical genetic studies established a link between Type 1 diabetes, a common childhood autoimmune disease and genes that encode MHC antigens and several immune-related determinants. The mechanisms by which these genes contribute to the initiation and perpetuation of Type 1 diabetes remain enigmatic. Emerging data indicate a role for epigenetic mechanisms involving hyperacetylation of histones in the differential gene expression and amelioration of autoimmune diabetes in a mouse model. In this article the implications of these and other epigenetic mechanisms including ncRNA-mediated gene regulation in the abrogation of autoimmune diabetes are discussed. Concerted efforts to decipher the epigenetics of Type 1 diabetes may provide novel perspectives on autoimmune diabetogenesis.