The role of the major histocompatibility complex of the mouse (H-2) in resistance to two transplanted histocompatible tumors was evaluated by determining the differences in survival times between the syngeneic parent strain and various F1 hybrids. C57BL/10nSn (B10) mice and their F1 hybrids were given injections of a methylcholanthrene-induced fibrosarcoma of B10 origin. The B10 × B10.BR F1, B10 × B10.M F1, B10 × B10.WB F1, and B10 × 5R F1 hybrids survived significantly longer than the B10 parental strain or B10 × B10.D2 F1 and B10 × 18R F1 animals, while B10 × 2R F1 mice succumbed significantly sooner than any of the above groups. Statistical comparisons of geometric mean survival times of the strain of tumor origin (B10) versus the F1 hybrids showed the influence of genes coded for the H-2 complex in the phenomenon, termed “hybrid resistance” or “allogeneic inhibition.” However, tumor resistance did not occur in all hybrids and could not be attributed to a single dominant Ir gene localized in the I region as might be predicted if the phenomenon involved genetic control of immunological responsiveness to tumor-specific transplantation antigens. Similarly, in a second group of experiments, the mean survival times of DBA/2 × B10.D2 F1 animals given injections of the P815 mastocytoma of DBA/2 (D2) origin was compared to the mean survival times of various hybrids with the D2 parent. Again, the results demonstrated the importance of the H-2 gene complex in this phenomenon. However, the above results did not permit precise localization of the H-2-linked gene(s) responsible for differential resistance to the histocompatible tumor.

1

Supported by National Cancer Institute Grant CA 14723.

This content is only available via PDF.