Cytotoxic T-cell responses in mice infected with influenza and vaccinia viruses vary in magnitude with H-2 genotype.

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Abstract
Secondary effector T[thymus-derived]-cell populations generated cross-priming with heterologous influenza A viruses operate only in H-2K or H-2D compatible situations, when assayed on SV40-transformed target cells infected with a range of influenza A viruses. The H-2Kb allele is associated with a total failure in the generation of influenza-immune cytotoxic T cells, though this is not seen for the primary response to vaccinia virus. In influenza and vaccinia development of effector T cells operating at H-2Db is greatly depressed in B10.A(24) (kkkddb) and B10.A(4R) (kkbbbb), but not in B10 (bbbbbb), mice. However, there is no defect in viral antigen expression at H-2Kk or H-2Db in B10.A(2R) target cells. This apparently reflects some inadequancy in the stimulator environment, as (A/J .times. B6) F1 T cells can be induced to respond at H-2Db when exposed to vaccinia virus in an irradiated B6 but not in a B10.A(4R) recipient. The 1st rigorous demonstration of a nonresponder situation and a probably Ir-gene effect for conventional infectious viruses is reported. Possible implications for the evolution of H-2 polymorphism and mechanisms of Ir gene function are discussed.

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