Abstract
Central to the normal immune response is the recognition of processed antigen by the cell-surface receptors of T lymphocytes. Within this interaction lies the capacity to discriminate appropriately between self and non-self antigens and to generate both specific and nonspecific responses against the antigens. Autoimmune disease results when the immune system fails to make this discrimination. There has been considerable progress recently1 in characterizing the target autoantigens against which autoimmune responses are directed, the immunologic mechanisms that induce autoimmune disease, and the immunogenetic backgrounds of persons at risk for the development of autoimmune disease. A major unresolved question remains — . . .