摘要：

The central pathogenic event in the development of autoimmune endocrine diseases is the immune-mediated destruction of the specific endocrine cell. In the case of autoimmune type 1 diabetes the cytotoxic destruction of the pancreatic islet β-cells occurs through apoptosis leading to inadequate insulin secretion and hyperglycemia. Immune-mediated apoptosis specifically triggered through #as, is believed to be central to the pathogenesis of autoimmune diabetes because this apoptotic mechanism destroys islet β-cells in both animal models of diabetes and the human type 1 disease. On the other hand, animals engineered to prevent Fas mediated cytotoxicity of islet cells do not develop the disease. Thus, apoptosis signaled through the Fas pathway appears to play an important role in the pathogenesis of autoimmune diabetes. The regulation of this pathway in the islet cells may alter the clinical expression of the disease.

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