Viral and immunological bases of beta cell failure in insulin-dependent diabetes

Pathologists have confirmed the specific nature of the insulitis lesion in diabetes requiring insulin. Data from genetic studies implicate both genetic and environmental influences as important in the appearance of overt disease. Certain HLA histocompatibility antigens are associated with insulin-dependent diabetes and have been interpreted as markers for closely linked immune response genes, a situation that may lead to beta cell susceptibility to viral injury or to uncontrolled beta cell autoaggression following beta cell damage. There is much circumstantial evidence that viruses may precipitate the disease (coxsackie) or may precede the disease onset by a long interval (mumps, rubella). However, susceptibility to virus, if it exists in human insulin-requiring diabetes, would appear on clinical grounds to be localized to the pancreas. Autoimmune phenomena are common in insulin-requiring diabetes, and there is both human and animal evidence that suggest that cell-mediated immunity may have a central pathogenic role. The recent explosion of new findings should lead to a clearer understanding of the nature of the disease, and this knowledge will hopefully lend itself to the prevention or arrest of the disease through immunological intervention, vaccination programs, or other means yet to be discovered.