Abstract
Progressive growth of the Meth A fibrosarcoma apparently evokes generation of a T[thymus-derived]-cell-mediated mechanism of immunosuppression that prevents this highly immunogenic tumor from being rejected by its immunocompetent host. Regression of large, established Meth A tumors could be caused by i.v. infusion of tumor sensitized T cells from the immune donors, but only if tumors are growing in T cell-deficient recipients. The adoptive T cell-mediated regression of tumors in such recipients can be prevented by prior infusion of splenic T cells from T cell-intact, tumor-bearing donors. The results leave little doubt that presence of suppressor T cells in T cell-intact, tumor-bearing mice is responsible for loss of an earlier generated state of concomitant immunity, and for the inablity of i.v. infused, sensitized T cells to cause tumor regression. Because presence of suppressor T cells generated in response to the Meth A did not suppress the capacity of Meth A-bearing mice to generate and express immunity against a tumor allograft, they were not in a state of generalized immunosuppression.