ABSTRACT
Insulin-dependent diabetes mellitus (IDDM) is a destruction of insulin-secreting cells within the islets of Langerhans of the pancreas. In the absence of pancreatitis or other pancreatic disease, the presence of antiislet cell autoantibodies and the association with some major histocompatibility complex alleles suggest that IDDM may involve autoimmune islet destruction. Associations with other autoimmune diseases and morphological evidence for islet inflammation first suggested that the immune system may be involved in the development of IDDM. IDDM is characterized by an absolute lack of insulin. Several models for autoimmune IDDM have been identified in laboratory animals. Two models will be discussed in detail because they summarize working hypotheses on the mechanism of disease development. Triggering events in human IDDM are unknown as is whether potential IDDM occurs due to intrinsic defects of the immune system or to environmental factors, i.e., infectious agents or chemicals. Autoreactive T- and B-lymphocytes and islet-specific autoantibodies are readily detected in IDDM patients.
