A/JCr mice reject SalN fïbrosarcoma cells genetically engineered to express major histocompatibility complex (MHC) class II molecules and are highly resistant to subsequent challenge with unmodified SalN cells. In this report we examine the mechanism by which this protective antitumor immunity is induced. We found that MHC class II antigen-positive tumor cells were no more effective than irradiated, MHC class II antigen-negative cells at inducing secondary protective immunity. Additionally, therapeutic immunization with MHC class II antigen-positive tumor cells had no effect on the growth of admixed SalN cells or preexisting SalN tumors. Based on these observations, we conclude that the MHC class II antigen-induced immune response is not related to SalN-specific antitumor immunity.

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