ABSTRACT
Autoimmune diseases result from self-reactive T-lymphocytes and autoantibodies, produced most likely in cooperation with T-cell dependent B-cells. Until recently, non-specific suppression of self-reactive lymphocytes or the inflammatory process mediated by the ongoing anti-self reactivity represented the main goal of therapy, but in the large majority of cases, neither cure nor remission can be obtained. Patients with severe, life threatening, manifestations of autoimmune diseases such as multiple sclerosis (MS), systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) may require long-term maintenance immunosuppressive treatment similar to organ allograft recipients, with all the anticipated side effects related to chronic immunosuppression on the one hand and side effects directly related to the immunosuppressive drugs (e.g., corticosteroids, cytotoxic agents and cyclosporin A to mention just a few) on the other. Unfortunately, none of the approaches available to date can offer effective and safe regulation of anti-self reactivity. Clearly, reinduction of unresponsiveness to-wards self antigens remains the yet unaccomplished final goal.
