Rejection of Mouse Renal Cell Carcinoma Elicited by Local Secretion of Interleukin‐2

We introduced the interleukin‐2 (IL‐2) gene into mouse renal cell carcinoma (RenCa) in order to examine the mechanism of tumor rejection. IL‐2 gene‐transfected RenCa (RenCa/IL‐2Hi) exhibited marked retardation of tumor growth when implanted in a syngeneic host. Growth retardation of RenCa/IL‐2Hi was also observed in athymic nude mice even after depletion of natural killer (NK) cells by treatment with anti‐asialo GM1 antibody. Histological analysis of RenCa/IL‐2Hi tumors disclosed non‐specific inflammatory changes in syngeneic hosts. Co‐injection of Bacillus Calmette Guerin with RenCa/IL‐2Hi considerably enhanced the anti‐tumor effects. Taken together, these findings strongly suggest that in situ IL‐2 production leads to tumor rejection through non‐specific inflammatory responses without participation of T cells and NK cells. On the other hand, the syngeneic mice that had rejected RenCa/IL‐2Hi acquired immunity against parental RenCa, suggesting possible participation of memory T cells in the second rejection of the tumor.