Involvement of complement in B-cell, T-cell and monocyte/macrophage activation.
In the early 70's it had been shown, that for the immune response against T-dependent antigens C3 was necessary, while T-independent antigens, although activating the alternative pathway of complement, triggered antibody formation also in C-deficient mice. During recent years functional and biochemical knowledge about complement binding structures on B-cells and monocytes/macrophages continuously increased and, also, on T-cells C3 binding entities have been detected. In the case of B-cells and, at least in special experimental conditions, in the case of T-cells C3 can exert a proliferative response as long as the cells are prestimulated (excited) by anti-Ig or IL-2, respectively. Monocytes can bind C3b- or iC3b-carrying particles, but only when progressed to macrophages can they phagocytose such particles. Thus the concept evolves that B-cells, T-cells and monocytes can acquire competence for a C3-driven response when excited properly. The involvement of molecules such as CR1, CR2, factor H, IL-2-receptor and others with a basic structure of repeating units of 61 amino acids in the triggering processes is a surprising finding and certainly suggests their functional importance. In the case of T-independent antigens the structures triggering the alternative pathway of complement are the structures triggering monocytes directly. Whether these two functions have a causal relationship has to be shown.
D000818:Animals; D000955:Antigens, T-Independent / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D003165:Complement System Proteins / Q000502:physiology*; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D008213:Lymphocyte Activation; D008262:Macrophage Activation; D009000:Monocytes / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D000955:Antigens, T-Independent; D000949:Histocompatibility Antigens Class II; D003165:Complement System Proteins