cAMP is an essential signal in the induction of antibody production by B cells but inhibits helper function of T cells.
Dibutyryl cAMP and IL 1 were found to stimulate antigen-specific and polyclonal antibody production when added together to cultures of highly purified B cells. We propose that IL 1 and an elevation in cytoplasmic cAMP represent minimal signal requirements for B cell activation. In contrast to its effect on B cells, dibutyryl cAMP inhibited helper T cell activity. Cyclic AMP suppressed the production of IL 2 and T cell replacing factor (TRF) by T cells and thus abrogated the ability of helper T cells to enhance SRBC-specific antibody production by B cells. Cyclic AMP did not inhibit the generation by T cells of B cell growth factor (BCGF). BCGF, not normally detected in Con A supernatant, was found in the culture supernatant of spleen cells that were stimulated with Con A in the presence of cAMP. Our findings indicate that cAMP blocks the production of an inhibitor of BCGF activity. cAMP had no effect on the production by macrophages of IL 1.
Gilbert
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Hoffmann
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D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology*; D003208:Concanavalin A / Q000276:immunology; D000242:Cyclic AMP / Q000502:physiology*; D007375:Interleukin-1 / Q000276:immunology; D007376:Interleukin-2 / Q000276:immunology; D008211:Lymphocyte Cooperation; D008222:Lymphokines / Q000276:immunology; D051379:Mice; D008819:Mice, Nude; D013154:Spleen / Q000293:injuries; D013601:T-Lymphocytes / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*
D007375:Interleukin-1; D007376:Interleukin-2; D008222:Lymphokines; D003208:Concanavalin A; D000242:Cyclic AMP