Viral and immunological bases of beta cell failure in insulin-dependent diabetes
N. K. Maclaren
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.