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.