Abstract
Madison lung carcinoma (M 109), a murine tumor of spontaneous origin, appears to be non‐immunogenic, according to commonly employed tests for tumor immunogenicity. However, C.parvum‐induced immunopotentiation during the growth of M109 tumor results in post‐excision anti‐tumor immunity to M109 tumor implants. The C.parvum‐potentiated post‐excision immunity to M109 is tumor‐specific and T‐cell‐dependent. T cells from mice whose progressive M109 tumors have been excised are capable, on passive transfer, of inhibiting adoptive immunotherapy of T‐cell‐deficient recipients by spleen cells from mice immunized with an admixture of M109 cells and C.parvum. The data are interpreted as evidence supporting the hypothesis that the apparent lack of anti‐tumor immunity in this tumor model is not due to the absence of tumor‐associated antigens. We suggest that, instead, in this model the balance between the effector and suppressor arms of the immune response favors tumor‐induced immunosuppression, resulting in a magnitude of anti‐tumor immunity insufficient for detection by commonly employed tests for tumor immunogenicity. Our study shows that shifting the balance in favor of the effector arm by means of immunopotentiation results in a measurable immune response to an apparently non‐immunogenic tumor.