Role of cytostasis in antitumor immunity against syngeneic X5563 plasmocytoma: comparative study of cytostasis and cytolysis using variant tumors and neonatally thymectomized mice.

The mechanism of antitumor immunity against syngeneic X5563 plasmocytoma was investigated with cytostasis and cytolysis assays by changing the host-tumor interrelationship using neonatally thymectomized (NTx) mice and spontaneous variant tumors. Immunization with mitomycin C-treated X5563 cells (MCC-X5563) in complete Freund's adjuvant (CFA) induced an effective anti-X5563 immunoprophylaxis in vivo. Such immunized mice and X5563 tumor-bearing mice showed cytostatic, but not cytolytic, activity in their peritoneal exudate cells (PEC) in vitro. Both cytostatic and cytolytic activities were induced in PEC of regressor (R1 and R2) variant tumor-bearing mice. But NTx mice, which could exert cytostatic activity and no cytolytic activity, could reject about one-half of R1 variant tumors. Immunizations using a progressor P1 variant tumor, obtained from R1 tumor after nearly complete rejection, did not give a prophylactic effect in vivo, nor did they induce in vitro cytolytic activity although a low degree of cytostatic activity was detected. These results suggest that cytostasis is the common and basic effector mechanism of antitumor resistance against syngeneic original or variant X5563 tumors, and that the collaboration of cytolysis and cytostasis exerts strong resistance against regressor variants.