Abstract
A CB6F1 murine T-cell hybridoma, FN1-18, secreting interleukin 2 in response to presentation of keyhole limpet hemocyanin (KLH) by syngeneic cells in the context of an I-E gene complementation product, also exhibited a major histocompatibility complex-restricted response to KLH presented by human leukocytes. The murine restriction element was I-E beta b or k E alpha d or k. The KLH-induced interleukin 2 production was inhibited by the monoclonal antibody 17-3-3s with similar but not identical anti-I-E specificity. This antibody reacted with human Ia-like antigens on T-depleted mononuclear cells in 10 of 30 humans, as assessed by immunofluorescence. The presence of the epitope recognized by antibody 17-3-3s was closely correlated with MT3 allospecificity. The ability of human cells to present KLH to the murine hybridoma strongly correlated (r = 0.768) with the expression of this epitope and was also inhibited by 17-3-3s. Another monoclonal antibody, 109d6, of the same isotype and with related but not identical MT3 specificity, caused only limited inhibition. The ability of human cells to present KLH segregated as a dominant trait linked to the major histocompatibility complex. The results indicate that the restriction element recognized by FN1-18 on both human and mouse cells is a determinant closely related to but not identical with the antigenic determinant to which 17-3-3s binds. This determinant is not influenced by the considerable species differences in the remainder of the Ia molecules.