NEW DIRECTIONS IN THE IMMUNOLOGY OF AUTOIMMUNE DIABETES

Human insulin-dependent diabetes mellitus is thought to be caused by a chronic autoimmune destruction of the islets of Langerhans, probably mediated by T cells. The association of the disease with major histocompatibility complex antigens most likely relates to the role of these antigens in presenting peptides to T lymphocytes. Once initiated, the autoimmune process can be detected in late, but preclinical stages, by autoantibodies and subtle defects in insulin secretion. Epitopes recognized by some autoantibodies have been identified, which will facilitate larger screening studies and the possibility of identifying individuals in earlier stages of the disease. The long-term results of trials of immunotherapeutic agents given to patients after onset have generally been disappointing, but the use of more specific, less toxic drugs and intervention at earlier stages of the disease have greater potential for arresting the autoimmune response. In the meantime, insulin itself has been found to help to preserve beta-cell function in patients with new-onset insulin-dependent diabetes mellitus, which has prompted many new questions about the immune pathogenesis and approach to treatment of this disease.