Camussi G, Salvidio G, Biesecker G, Brentjens J, Andres G
Department of Pathology, State University of New York, Buffalo 14214.
J Immunol. 1987 Nov 1;139(9):2906-14.
The aim of this study was to investigate the in vitro role of the complement membrane attack complex (MAC) in the injury induced by nephritogenic anti-brush border vesicle (Fx1A) antibodies on rat glomerular visceral epithelial cells (GEC). Both sheep and rabbit anti-rat brush border vesicle IgG-induced complement-dependent lysis of cultured GEC. Fab fragments of sheep anti-rat brush border vesicles and polyclonal or monoclonal gp330 IgG were devoid of lytic activity. Shedding of cell-surface antigens induced by sheep or rabbit anti-rat brush border vesicle IgG protected GEC from subsequent exposure to lytic antibodies and complement, an effect that was not obtained with Fab fragments. When GEC were incubated with sheep or rabbit anti-rat brush border vesicle IgG in capping conditions, the C3 component was co-redistributed with Heymann immune complexes; in contrast, the MAC remained diffusely bound to the cell surface, indicating that it was not associated with the antigen-antibody complexes. The MAC was demonstrated on the surface of GEC by immunofluorescence staining with anti-MAC neoantigen and by electron microscopy of negatively stained membranes showing focal clusters of 110 A MAC lesions. When GEC were treated with sheep IgG or rabbit IgG plus C6-deficient sera, the cells were not lysed and MAC was not demonstrable on the surface; however, lytic activity was restored when C6-deficient sera were reconstituted with purified C6. The results are consistent with the interpretation that injury induced by Heymann antibodies on GEC is MAC-dependent.
本研究的目的是探讨补体膜攻击复合物(MAC)在致肾炎性抗刷状缘囊泡(Fx1A)抗体诱导的大鼠肾小球脏层上皮细胞(GEC)损伤中的体外作用。绵羊和兔抗大鼠刷状缘囊泡IgG均可诱导培养的GEC发生补体依赖性溶解。绵羊抗大鼠刷状缘囊泡的Fab片段以及多克隆或单克隆gp330 IgG均无溶解活性。绵羊或兔抗大鼠刷状缘囊泡IgG诱导的细胞表面抗原脱落可保护GEC免受后续溶细胞性抗体和补体的作用,而Fab片段则无法产生这种效果。当GEC在帽化条件下与绵羊或兔抗大鼠刷状缘囊泡IgG孵育时,C3成分与海曼免疫复合物共同重新分布;相反,MAC仍分散地结合在细胞表面,表明它与抗原-抗体复合物无关。通过抗MAC新抗原的免疫荧光染色以及负染膜的电子显微镜观察显示11 nm MAC损伤的局灶性聚集,证实了GEC表面存在MAC。当用绵羊IgG或兔IgG加C6缺陷血清处理GEC时,细胞未被溶解,且表面未检测到MAC;然而,当用纯化的C6重建C6缺陷血清时,溶解活性得以恢复。这些结果与海曼抗体诱导的GEC损伤依赖于MAC的解释一致。