Type 1 diabetes mellitus is a serious health problem that affects several million new people each year. Although it is recognized that type 1 diabetes results from an autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans, its etiopathogenesis is still not well understood. A certain genetic phenotype seems to be required, but it is not sufficient per se to trigger diabetes development. Numerous studies have pointed to the role of infectious agents as important environmental factors in breaking 'self'-tolerance and triggering activation of autoreactive T cells. Activated T cells, in turn, destroy target cells harboring the corresponding tissue-specific self-antigen, causing organ damage and loss of function. Several theories have been proposed to explain how environmental factors can initiate and/or perpetuate autoimmunity towards pancreatic beta-cells.
Copyright 2000 S. Karger AG, Basel