REGULATION OF ANTIBODY-PRODUCTION BY HELPER T-CELL CLONES IN EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS IS MEDIATED BY IL-4 AND ANTIGEN-SPECIFIC T-CELL FACTORS

Acetylcholine receptor (AChR)-specific rat T cell clones (CD4+, CD8-, and OX22-) were shown to secrete both Th1 and Th2 lymphokines, IL-2, IL-4, and IFN-γ following stimulation with AChR. These clones helped production of antibody to AChR by B cells which was found to be regulated primarily by IL-4, not by IL-2, secreted by the T cells in response to AChR. Cell-free supernatants from some AChR-activated T cell clones led to production of low levels of antibody to AChR by B cell-enriched, AChR-primed lymph node cells. Supernatant-regulated help in antibody production by B cells was antigen specific, and antibodies to T cell receptors blocked the antigen-specific activity. Thus, supernatant-mediated help may not be due solely to IL-4, and other factors, possibly including some fragment of the T cell antigen receptor present in the supernatant, appear to contribute to helping antibody production by B cells. © 1993 Academic Press, Inc.