Abstract
Type 1 diabetes, also referred to as insulin-dependent diabetes mellitus (IDDM), is an autoimmune disorder resulting from the destruction of pancreatic beta-cells and insulin deficiency. In the last 10 years significant progress has been made in this field, primarily because of the identification of predisposing genes, the extensive investigation of animal models, and the characterization of major autoantigens. This review draws attention to how the study of beta-cell autoantigens may contribute insight into the pathogenesis of IDDM and provides an update on the cell biology of glutamic acid decarboxylase (GAD) and islet cell autoantigen 512, two major targets of autoimmunity in Type 1 diabetes on which I have focused my efforts. For reasons of space I have mostly considered here studies on GAD which have been published since 1994.
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