Adoption of tumor immunity: role of the major histocompatibility complex.

T cells from spleens of mice immunized against a chemically induced tumor were able, when transferred to normal syngeneic mice together with tumor cells, to protect adoptively against tumor growth. The inability of such cells to identically protect pangenic nude mice and F1 hybrid mice, and the incompetence of T cells alone in the in vitro tests indicated that the T cells by themselves were unable to kill the tumor cells. We hypothesized that the protection transmitted by spleen T cells results from an interaction with the recipient mouse and that this interaction is controlled by the major histocompatibility complex (MHC). Analysis of the lack of protection at the level of the MHC subregion demonstrated that in the transfer of immune spleen T cells from parent mice to F1 recipient mice, an identity of the KIA subregion permitted a complete transfer of protection. In the transfer of immune spleen T cells from F1 mice to parent recipients, a semi-identity of the KIA subregion was sufficient but a complete identity of the H2D subregion was necessary. The use of such a model, requiring the transfer of parental cells to F1 hybrid mice, necessitated the analysis of the possible role of the hybrid resistance gene. We have demonstrated the absence of correlation between the hybrid resistance and the adoptive protection. At the present stage of this work, the adoptive neutralization test allows us to conclude that the immunologic rejection of a chemically induced tumor is the result of interaction between 2 cells, a T cell and a radioresistant non-T cell.