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.
D000818:Animals; D000912:Antibodies, Neoplasm / Q000032:analysis; D003601:Cytotoxicity Tests, Immunologic; D004900:Erythroblasts; D004906:Erythrocyte Count; D007109:Immunity; D007111:Immunity, Cellular; D007942:Leukemia, Experimental / Q000276:immunology* / Q000473:pathology; D008099:Liver / Q000473:pathology; D051379:Mice; D008811:Mice, Inbred DBA; D009365:Neoplasm Regression, Spontaneous; D011925:Rauscher Virus; D013154:Spleen / Q000473:pathology; D013163:Splenomegaly
D000912:Antibodies, Neoplasm