Interleukin-2 production in response to phytohemagglutinin is not necessarily dependent upon the T3-mediated pathway of T-cell activation.
The present study was designed to investigate whether heterogeneity exists in the requirement for T3 molecules in the mechanism of T-cell activation and interleukin-2 (IL-2) release by IL-2-producing T-cell clones. Clones were derived from peripheral blood by a culture system which allows clonal expansion of essentially all T lymphocytes or from mixed lymphocyte culture (MLC) activated T-cell population. IL-2-producing clones were selected and cell aliquots treated with anti-T3 monoclonal antibodies (mAb) to induce modulation of T3 surface molecules. Although stimulation of modulated clones with different anti-T3 mAb did not lead to IL-2 production, 4/39 of these clones produced IL-2 after stimulation with phytohemagglutinin (PHA). The ability of these clones to be activated by PHA could not be explained by incomplete T3 modulation. In addition, two alloreactive clones were isolated from MLC population in which modulation of T3 antigens abrogated the IL-2 production induced by either anti-T2 mAb or allogeneic stimulation but had no effect on PHA-induced IL-2 release. These data further support the concept that PHA may trigger some T cells via surface molecules that are independent from the T3-Ti cell receptor molecular complex.
D000911:Antibodies, Monoclonal; D000954:Antigens, Surface / Q000276:immunology; D002999:Clone Cells; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis*; D008213:Lymphocyte Activation / Q000187:drug effects*; D010835:Phytohemagglutinins / Q000494:pharmacology*
D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D007376:Interleukin-2; D010835:Phytohemagglutinins