A novel role for interleukin 2 in antibody responses: down-regulation of T helper cell activation.
This report provides new insights into the role of the T cell growth factor interleukin 2 (IL 2) for the regulation of antibody responses. Evidence is presented that IL 2 down-regulates T helper cell (Thc) activation but not Thc effector function, i.e., Thc-B cooperation. Thus, reagents which block the IL 2 pathway, e.g., cyclosporin A (CsA) or IL 2 receptor monoclonal antibodies (IL 2R Mab) enhanced Thc activation although T cell proliferation was blocked. In contrast, CsA or IL 2R Mab blocked Thc-B cooperation, suggesting that IL 2 is required for this step. The regulatory role of IL 2 was reconfirmed by the addition of exogenous IL 2 into the cultures which reversed the enhancing or blocking effect of CsA.
D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D001402:B-Lymphocytes / Q000276:immunology; D003524:Cyclosporins / Q000494:pharmacology; D007376:Interleukin-2 / Q000502:physiology*; D008213:Lymphocyte Activation / Q000187:drug effects; D008211:Lymphocyte Cooperation / Q000187:drug effects; D051379:Mice; D008807:Mice, Inbred BALB C; D011971:Receptors, Immunologic / Q000502:physiology; D015375:Receptors, Interleukin-2; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*
D003524:Cyclosporins; D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2