Role of Different T Cell Sets in the Rejection of Syngeneic Chemically Induced Tumors

Abstract

This study was designed to investigate the phenotypes of immune cells concerned in the rejection of chemically induced tumors. Counted numbers of viable dissociated cells of a selected C57BL/6 (B6) tumor were combined with counted numbers of peritoneal cells from highly immunized syngeneic B6 donors and inoculated subcutaneously into untreated syngeneic B6 mice. Progressive tumor growth was prevented by nonadherent immune peritoneal cells in numbers less than one-quarter the number of tumor cells, and the cells responsible belonged mainly or entirely to the nonadherent fraction of the peritoneal population. There was no cross-protection between this tumor and a second B6 tumor induced by the same carcinogen, indicating that immunity in this experimental system, as reported previously, is directed to antigens that individually characterize chemically induced tumors. Elimination of Thy-1(+) cells by Thy-1 antiserum and complement abolished the protective capacity of the immune peritoneal cells, showing that immunity under these conditions is mediated by T cells. Protection was also precluded by elimination of Lyt-1(+) cells or of Lyt-2(+) cells, showing that protection could not be attributed to either the Lyt-23 or the Lyt-1 set of T cells alone. Nor was protection conferred by various combinations of these selected Lyt-1 and Lyt-23 cell sets. Thus, participation of the third well defined Lyt cells set, Lyt-123, which is automatically eliminated when the Lyt-23 and Lyt-1 sets are prepared by selective immune cytolysis is evidently necessary to rejection, in these experimental circumstances. Although this might imply that cytotoxicity for syngeneic tumors is effected by Lyt-123 cells, it is emphasized that this assay system allows time for the differentiation and proliferation of cells sets. Thus, the data are also consistent with a uniform hypothesis that cell-mediated cytotoxicity is an exclusive function of Lyt123:CS cells, and that these, and possible Lyt1:H amplifier cells, are generated in the course of the assay from a specifically primed antecedent Lyt123:ARC cell set.