Abstract
The ability of murine helper T [thymus-derived] cells primed to the antigen, sheep erythrocytes (SRBC), to cross-react with burro erythrocytes (BRBC) in the in vitro antitrinitrophenol (TNP) response to TNP-RBC was shown to be under genetic control. Although non-H-2 genes influenced the absolute level of helper activity assayed after SRBC priming, the extent of cross-reaction of SRBC-primed helpers with BRBC was controlled by an H-2-linked Ir gene(s). H-2 haplotypes were identified which determined high, intermediate, or low response to the cross-reacting determinants and the gene(s) controlling the cross-reaction tentatively mapped to the K through I-E end of the H-2 complex. Helpers primed in F1 mice of high .times. intermediate or high .times. low responder parents were tested for cross-reaction using B [bone marrow-derived] cells and macrophages (M.PHI.) of parental haplotypes. In each case the extent of cross-reaction was predicted by the H-2 haplotype of the B cells and M.PHI., establishing the expression of the Ir gene(s) in B cells and/or M.PHI. at least, but not ruling out its expression in T cells as well. The low cross-reaction seen when T cells from F1 mice of high .times. low responder parents were tested on low responder B cells and M.PHI. was not increased by the presence of high responder M.PHI., indicating the Ir gene(s) is expressed in the B cell at least although it may be expressed in M.PHI. as well. These and the previously reported experiments are consistent with the hypothesis that helper T cells recognize antigen bound to the surface of B cells and M.PHI. in association with the product(s) of Ir gene(s) expressed on the B cell and M.PHI.

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