The role of complement in the induction of acute antibody-mediated vasculitis of rat skin grafts in the mouse.
Rat skin grafts carried by immunosuppressed mice can be acutely destroyed by intravenous administration of mouse anti-rat antibody. The velocity of the reaction and the histologic sequence of events depend on the amount of antibody administered: low doses give an Arthus-like rejection, whereas at high doses a Shwartzman-like pattern occurs. Depletion of C3 by cobra venom factor treatment did not prevent acute rejection after intravenous injection of high doses of antiserum but changed the reaction from a Shwartzman-like to an Arthus-like pattern. Conversely, supplementary administration of rabbit complement caused a violent Shwartzman-like graft destruction after injection of low doses of antibody, which in complement-normal mice gave an Arthus-like reaction. The results show that complement can greatly amplify the antibody-mediated immune vasculitis and can substantially modify its histologic pattern. It is, however, not an absolute requirement for the occurrence of the destructive process.
D000208:Acute Disease; D000818:Animals; D000906:Antibodies / Q000008:administration & dosage / Q000276:immunology*; D003165:Complement System Proteins / Q000502:physiology*; D004546:Elapid Venoms / Q000494:pharmacology; D006084:Graft Rejection; D007108:Immune Tolerance; D051379:Mice; D008810:Mice, Inbred C57BL; D018366:Vasculitis, Leukocytoclastic, Cutaneous / Q000276:immunology*
D000906:Antibodies; D004546:Elapid Venoms; C016310:cobra venom factor; D003165:Complement System Proteins