Immune response genes control T killer cell response against Moloney tumor antigen cytolysis regulating reactions against the best available H-2 + viral antigen association.

Abstract

Cytolytic T [thymus-derived] lymphocytes (CTL) specific for the virus-induced and leukemia-associated Friend, Moloney, Rauscher (FMR) antigen are easily detected in the spleens of primary and secondary stimulated H-2b or H-2d mice. They react, respectively, with H-2Db + FMR and H-2Kd + FMR, Dd and Kb never being involved. Recombinant (KbDd) mice are relatively low responders that produce CTL only after secondary stimulation. Competition and blocking experiments with monospecific anti-H-2 antibodies demonstrated that on the same H-2b tumor cells, C57BL/6 (H-2b) lymphocytes recognize Db + FMR, whereas B10.A(5R) lymphocytes recognize Kb + FMR. The restriction cannot be explained by a specific association of viral molecules with certain H-2 products. The CTL response of (B10 .times. 5R)F1 hybrids is easily detected in primary reaction, the high responder anti-FMR phenotype being dominant, and directed against Db + FMR, F1 mice being low responder against Kb + FMR like the B10 parent. A D region-associated immune response gene apparently controls the cell-mediated anti-FMR reaction, the best available H-2 + FMR antigenic association being chosen by CTL precursors.