Cell‐mediated cytotoxicity against ectromelia virus‐infected target cells. III. Role of the H‐2 gene complex

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Abstract
The role of the H‐2 gene complex in expression of cytotoxicity exerted by specific ectromelia‐immune thymus‐derived (T) cells against ectromelia‐infected target cells was examined. A repertoire of inbred mouse strains (some congenic) including the H‐2 haplotypes k, d, b, s, q, the recombinant H‐2a (k|d) and F1 hybrids (k/b and d/b) were immunized with virus and their spleen cells tested 6 days later, at the peak of the primary response, against H‐2k, H‐2d and H‐2b target cells. Significant specific cytotoxicity occurred only when the immune cell donors and the target cells shared all or part of the same H‐2 gene complex. For example, H‐2a (k|d) immune cells killed both H‐2k and H‐2d target cells. There wasno detectable effect of the non‐H‐2 genetic background, H‐2 public specificities, or the M‐locus Target cells infected with ectromelia virus exhibited quantitative or qualitative changes (or both) in expression of normal H‐2 antigens as indicated by reduced susceptibility to killing by T cells activated against H‐2 antigens in mixed lymphocyte culture. These data are consistent with the hypothesis that T cells in this system are responding to virus‐induced, specific changes in antigens on infected cells which are controlled by genes in the H‐2 complex; these genes seem likely to be those coding for H‐2 private specificities, or genes closely linked to them.