Immune Intervention in Diabetes: State of the Art and Future Directions

The suggestion that insulin-dependent diabetes mellitus (IDDM) in humans results from the destruction of pancreatic beta-cells by an autoimmune process depends on three main lines of evidence. First the association of IDDM with markers of the major histocompatibility complex (MHC) indicates not only that genetic factors are important in determining susceptibility to the disease but also that this may be related to immune system functions.1,2 Second the disease is associated with evidence of antibody-mediated and cell-mediated immunologic reactions during progression to insulin dependence.3–5 Third the inflammatory process in the islets of Langerhans in IDDM is consistent with the autoimmune hypothesis and perhaps is best exemplified by pancreas transplantation in discordant identical twins, during which the histology of the pancreatitis that occurs in the recipient in the absence of immunosuppression has been studied.6 Investigations concerning each of these lines of evidence continue, as discussed elsewhere in this volume.