부산대학교 도서관

Breakdown of C3 by hypocomplementæmic sera from patients with mesangiocapillary nephritis (M.C.G.N.) was shown to be mediated by the alternative pathway of complement activation. Evidence indicated that a fragment of C3 (C3b) is required for activation of the alternative pathway in nephritic serum. It is concluded that depletion of C3 in patients with M.C.G.N. is responsible for the known failure of their sera to break down pure C3 and for the normal survival of radio-labelled C3 preparations observed in such patients. These observations clearly demonstrate the activation of the complement system by the alternative pathway in human disease.