AbstractEstablished, H‐2 incompatible, mouse skin allografts are destroyed in 24–48 h by a single intravenous injection of specific alloantibody and heterologous complement (C) from rabbits (RC), guinea pigs (GpC) or humans (HC). Mouse complement (MC) itself is inefficient in this respect since grafts are not destroyed by the injection of antibody alone. This is in keeping with the low efficiency of MC inin vitrocytolysis.We have studied the role of different C factors in this model. Two patterns were observed. (a) Three C‐deficient sera (GpC‐R4, GpC‐R3, RC‐R6) showed neither activityin vitro(C‐mediated lymphocytotoxicity in a trypan blue assay) nor did they induce graft destruction. Activityin vitroandin vivocould be completely reconstituted with the appropriate C component. (b) Two C‐deficient sera (GpC‐R1 and HC‐R9) were inactive inin vitrocytotoxicity but, nevertheless, induced destruction of the skin grafts if injected with antibody. Thus,in vivo, the mouse seemed to provide the deficient factor, and this was confirmed by the observation thatin vitrocytotoxicity could be reconstituted not only with the appropriate C component, but also with normal mouse serum. The results show that the inefficiency of MCin vitroandin vivodoes not reside in the factors C1 or C9. Furthermore, in our model C is activated via the classical pathway, and at least exogenous C4, C3 and C6 are required to induce acute antibody‐mediated graft destruction.From the experiments with C6‐deficient serum which has normal chemotactic properties, it is concluded that activation of chemotactic factors with attraction of granulocytes is not sufficient to induce rejection, but that the activation of the membrane
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