Down-Regulation of the Antitumor Immune Response

TLDR: It is suggested that down-regulation of antitumor immunity by suppressor T cells can explain the escape of only of those tumors that are immunogenic enough to evoke the generation of enough effectors T cells to cause tumor regression in the absence of suppressing T cells.

Abstract: Publisher Summary This chapter discusses the immune response to chemically induced, transplantable tumors in syngeneic mice. It deals with those tumors that are immunogenic by virtue of their possession of tumor-specific, transplantation rejection antigens. A framework of evidence has been presented in the chapter that supports the hypothesis of down-regulation of antitumor immune response. Direct evidence for the hypothesis consists of the finding that infusion of suppressor spleen cells from donors with a large tumor can prevent recipient mice from generating a concomitant immune response. Additional direct evidence is being supplied by an ongoing study that shows that complete or partial regression of the Meth A fibrosarcoma that results from appropriately timed exposure to sublethal, whole-body γ-radiation is associated with a prolonged generation of effector T cells and an absence of suppressor T cells. It is suggested that down-regulation of antitumor immunity by suppressor T cells can explain the escape of only of those tumors that are immunogenic enough to evoke the generation of enough effectors T cells to cause tumor regression in the absence of suppressor T cells. This implies that the immunity generated to some tumors is too little too late to cause regression, even in the absence of the negative regulatory influence of suppressor cells. Therefore, successful immunotherapy of some established tumors, besides depending on the employment of agents capable of eliminating suppressor T cells, will also depend on the employment of agents capable of directly augmenting the generation of effectors T cells.