Rous sarcoma virus-induced tumours in mice. II. Contribution of H-2 and non-H-2 alloantigen barriers to tumour immunogenicity in vivo.

The features of the immune recognition of a murine fibrosarcoma induced by Rous sarcoma virus were tested in histocompatible and histoincompatible mice. No evidence of a genetic regulation of spontaneous reactivity to tumour-associated antigens was found in various histocompatible F1 hybrids. Incompatibility in multiple minor histocompatibility antigens triggers a host reaction incapable of causing tumour rejection in some cases. The growth rate of incipient tumours is unaffected, whereas that of already visible tumour masses is significantly delayed. Admixture to the challenge of inactivated leukocytes bearing the same minor histocompatibility antigens as the tumour triggers a significantly stronger reaction. The reaction of hosts incompatible in the H-2K or H-2DL regions is quite efficient. However, the intensity of the immune reaction of H-2DLs antigens displayed by tumour cells is markedly dependent on the alleles of genes located in the central regions of the H-2 complex.