Role of endogenous complement in monoclonal IgM antibody-dependent leukemia suppression in vivo: participation of C3b.
The mechanism by which McAb of the IgM isotype causes prolonged survival of leukemic rats was investigated. The participation of endogenous C in the suppression of IgM-sensitized leukemia cells was demonstrated by the observations that a) suppression was abrogated in CVF-treated rats, and b) the CVF effect was partially reversed if C3b was provided on the surface of IgM-sensitized leukemia cells.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000502:physiology*; D000920:Antibody-Dependent Cell Cytotoxicity; D001666:Binding Sites, Antibody; D003179:Complement C3b / Q000378:metabolism / Q000502:physiology; D003165:Complement System Proteins / Q000502:physiology*; D004546:Elapid Venoms / Q000494:pharmacology; D006801:Humans; D007108:Immune Tolerance; D007075:Immunoglobulin M / Q000378:metabolism / Q000502:physiology*; D007700:Kinetics; D007938:Leukemia / Q000276:immunology* / Q000378:metabolism / Q000628:therapy; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D051381:Rats
D000911:Antibodies, Monoclonal; D004546:Elapid Venoms; D007075:Immunoglobulin M; C016310:cobra venom factor; D003179:Complement C3b; D003165:Complement System Proteins