Studies of the biologic effects of selective C4 deficiency.
The role of the several pathways of complement activation in mediating a number of the biologic activities of complement has been examined in an animal model, the C4-deficient guinea pig. It has been shown that the presence of an intact classic pathway (C1, 4, 2) is requisite for damage of antibody-sensitized mammalian cell membranes and for the development of thrombocytopenia and the hypercoagulable state following in vivo endotoxin administration. Both the classic and alternate pathways participate in defense against the lethal effects of endotoxin, in opsonization and lysis of bacteria and in mediation of the events of inflammation.
D000936:Antigen-Antibody Complex; D001419:Bacteria / Q000276:immunology; D001433:Bacteriolysis; D001777:Blood Coagulation; D001780:Blood Coagulation Tests; D001792:Blood Platelets; D002462:Cell Membrane; D002633:Chemotaxis; D003181:Complement C4 / Q000172:deficiency*; D003165:Complement System Proteins / Q000172:deficiency* / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology; D006801:Humans; D013921:Thrombocytopenia / Q000209:etiology
D000936:Antigen-Antibody Complex; D003181:Complement C4; D004731:Endotoxins; D003165:Complement System Proteins