Mice bearing late-stage tumors have normal functional systemic T cell responses in vitro and in vivo

Immune suppression in tumor-bearing hosts is considered to be cane factor c ausally associated with the growth of antigenic tumors. Support for this hy pothesis has come from reports that spleen T cells in tumor-hearing mice ar e deficient in either priming or effector phase functions, We have reexamin ed this hypothesis in detail using multiple murine tumor models, including transplantable adenocarcinoma, melanoma, sarcoma, and thymoma, and also a t ransgenic model of spontaneous breast carcinoma. In both in vitro and in vi vo assays of T cell function (proliferation, cytokine production, induction of CD8(+) alloreactive CTL, and development of anti-keyhole limpet hemocya nin CD4(+) T cells, rejection of allogeneic or syngeneic regressor tumors, respectively) we show that mice bearing sizable tumor burdens are not syste mically suppressed and do not Rave diminished T cell functions. Therefore, if immune suppression is a causal function in the growth of antigenic tumor , the basis for escape from immune destruction is likely to be dependent up on tumor-induced T cell dysfunction at the site of tumor growth.