Defective cytotoxic T-cell generation in Moloney murine sarcoma virus-infected A/Sn mice

Cytotoxic T-cells (CTL) could not be detected in spleen cell suspensions from Moloney murine sarcoma virus (M-MuSV)-induced tumor-bearing A/Sn and (A/Sn X C57BL/6) F1 mice, with the A/Sn-derived natural killer (NK)-sensitive YAC-1 lymphoma cells used as targets. However, spleen T-cells from tumor-bearing (A/Sn X C57Bl/6)F1 mice were efficient killers against C57BL/6-derived RBL-5 cells. When tested for viral antigens by sera from mice with regressing atumors, YAC-1 and RBL-5 cells cross-reacted. The anti-RBL-5 effect of spleen cells from A/Sn X C57BL/6)F1 tumor bearers was blocked in cold target competition experiments by YAC-1 cells, which suggested the expression of a CTL target structure on YAC-1 cells. The activity against YAC-1 cells in spleen suspensions of both tumor-bearing and control (A/Sn X C57BL/6)F1 mice seemed to be an NK phenomenon entirely, because blocking occurred neither with RBL-5 cells nor with freshly prepared YAC lymphoma cells, both of which have low sensitivity to NK effects. Spleen cells from (A/Sn X C57BL/6)F1 regressors were stimulated to a secondary CTL response in vitro by YAC-1 and RBL-5 cells, which further indicated that YAC-1 cells express the M-MuSV-specific CTL target structure. These experiments also showed that YAC-1 cells could be lysed by CTL. YAC-1 cells did not induce a secondary response in A/Sn regressors, which indicated a lack of M-MuSV-induced CTL memory cells in this strain. The result was not due to a general unreactivity of A/Sn mice against YAC-1 cells, because spleen cells from YAC-1-immunized mice exhibited strong T-cell-mediated anti-YAC-1 activity after in vitro cultivation. Thus tumor regression seems to occur without the production of CTL in A/Sn mice.