Mechanism of resistance of mice to syngeneic methylcholanthrene induced fibrosarcomas.

Mice become resistant to challenge with certain fibrosarcomas when bearing a tumor graft (concomitant immunity) or after injection of a low, non-tumorigenic dose of cells (sinecomitant immunity). Resistance to footpad challenge was depressed or abolished by treatment with carrageenan, niridazole or reserpine, or by sublethal irradiation, all of which also depressed delayed-type hypersensitivity (DTH) reactions. Immune lymphocytes initiating tumor-suppressive reactions in the feet of non-immune mice were Thy-1+, Ly-1+, Ly-2- and Ly-3-. Injection of tumor cells into the peritoneal cavities of immune mice specifically elicited an influx of macrophages. There was evidence of macrophage stimulation in tumor-immune mice. In vitro, anti-tumor effector cells lacking individual tumor specificity could be detected among the resident peritoneal cells of tumor-immune mice and among peritoneal exudate cells of non-immune mice. The expression of acquired resistance to some tumors may involve reactions akin to DTH in which a specific reaction triggers an accumulation of nonspecific effectors.