Immune response to rauscher virus-induced leukemia in DBA mice. I. Role of cellular and humoral immunity in spontaneous regression.

DBA/1 and DBA/2 mice infected with the Rauscher leukemia virus developed a biphasic erythroleukemia. Transitory regression of the disease was closely associated with the appearance of tumor-specific antibodies and the exacerbation was preceded by the gradual decrease of antibody titer. The antibody-dependent cellular cytotoxicity could be detected earlier, than the complement-dependent cytotoxicity. Moreover, in each case the titer of antibody-dependent cellular cytotoxicity was higher than that of complement-dependent cytotoxicity. The results suggest that the antibody-dependent cellular cytotoxicity is mainly responsible for the rejection of tumor cells.