The ability to distinguish" self" from" non-self" is central to the normal function of the immune system. An essential condition for self-nonself discrimination is the immunological tolerance to self components. The mechanisms underlying the development and maintenance of self-tolerance are thought to involve one or more of the following:(i)" clonal deletion" or" clonal anergy" of relevant effector cells (1-5),(ii) active regulation through T-suppressor cells (6-10),(iii) regulation through idiotypic net works (11-14), and (iv) sequestering of self-antigens (15, 16). If the mech anisms regulating self-tolerance break down, an excessive immune response against a self-antigen sets in, sometimes resulting in a pathological condition or an autoimmune disease.

Autoimmune diseases affect at least 2% of the US population with a myriad of presentations including rheumatoid arthritis, insulin-dependent diabetes, systemic lupus erythematosus, myasthenia gravis, multiple scle rosis, and pemphigus vulgaris. For many of these diseases, the events which result in end organ damage are known; however, little is known about how an autoimmune response is activated and perpetuated. Most of the early studies focused on B cells and autoantibodies (17-25). With the recent advent of new methodologies for studying T cells, there is now compelling evidence that helper T cells play a pivotal role in the activation of the autoimmune response (26-30). This article reviews the role played by T lymphocytes in the effector phase of autoimmune diseases. In particu-