The role of complement receptors in tumor cell destruction.
Murine peritoneal macrophages exuding early after stimulation with the activators of the alternative complement pathway are able to destroy some of the tumor cells. This destruction is inhibited by anti-Mac-1 and anti-C3. The tumor cell killing needs longer incubation time (> 15 hr), and anti-Mac-1 affects the reaction even if it were put into the reaction mixture at later time of incubation. The results suggest that complement produced by macrophage is deposited onto target cells, and the complement binding targets interact with macrophages through the complement receptor type 3 (CR3), which leads to the cell destruction. It is known that fully activated macrophages kill the tumor cells with the aid of antibody (ADCC) or lectin, but we show here another route of tumor cell destruction, that is, some sort of incompletely activated macrophages can kill some type of tumor cells in cooperation with endogenous complement and complement receptors (CR3) without participation of antibody.
Okuda
T
T
Department of Immunology, Tohoku University, Sendai, Japan.
Tachibana
T
T
D000818:Animals; D003176:Complement C3 / Q000096:biosynthesis*; D003602:Cytotoxicity, Immunologic / Q000502:physiology*; D016177:Macrophage-1 Antigen / Q000502:physiology*; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D008809:Mice, Inbred C3H; D014407:Tumor Cells, Cultured
D003176:Complement C3; D016177:Macrophage-1 Antigen