The possibility that pancreatic beta cell destruction leading to type 1 diabetes is initiated by the release of cytokines by polyclonal activation of the immune system.

The cause of the destruction of the insulin-producing beta cells leading to type 1 diabetes is still unknown. Over the last few years it has become clear that autoimmune abnormalities, such as insulitis, autoantibodies against islet cell antigens and cellular cytotoxicity to beta cells are associated with the onset of type 1 diabetes. Nevertheless, it is still uncertain whether immune phenomena observed in human beings correspond to primary or secondary events in the development of type 1 diabetes. We do not know why the process of becoming diabetic is so lengthy in a risk proband with a genetic and immunological predisposition. Whatever the explanation of genetic association to the pathogenesis of type 1 diabetes may be, it seems sure that environmental factors may decisively influence the outcomes. In this article we summarize evidence implying that cytokines released during polyclonal activation of the immune system may initiate the beta cell destruction leading via autoimmune mechanisms of beta cell killing to insulin-dependent diabetes mellitus.