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系统性红斑狼疮性肾炎中膜攻击复合物的肾脏定位

Renal localization of the membrane attack complex in systemic lupus erythematosus nephritis.

作者信息

Biesecker G, Katz S, Koffler D

出版信息

J Exp Med. 1981 Dec 1;154(6):1779-94. doi: 10.1084/jem.154.6.1779.

Abstract

The membrane attack complex (MAC) of the complement system was localized in both glomeruli and peritubular regions of 22 kidneys manifesting systemic lupus erythematosus (SLE) nephritis. A similar distribution was observed for immune complex markers (IgG, Clq, and C3) and MAC in glomeruli, although the deposits of MAC were more discrete and showed lesser immunofluorescence staining intensity compared with immunoglobulins and complement components. In contrast, peritubular immune complexes were present in only 7 out of 22 kidneys, involved comparatively small clusters of tubules, exhibited weaker immunofluorescence staining than MAC, and failed to correlate with interstitial foci of inflammation. Granular or irregular, linear aggregates of the MAC were observed at the periphery of larger groups of tubules contiguous to areas of interstitial inflammation. Comparable amounts of IgG, Clq, C3, and MAC were present in blood vessel walls in areas of fibrinoid necrosis. These data suggest that the MAC is a direct mediator of tissue injury occurring in renal glomeruli, tubules, and blood vessels. The discordance between immune complexes and MAC localized in the peritubular region, but not in glomeruli or blood vessels, raises the possibility that both immune complexes and nonimmune agents, such as bacterial antigens, may activate the classical or alternative complement pathways and thereby play a role in the pathogenesis of tubulointerstitial lesions of SLE nephritis.

摘要

补体系统的膜攻击复合物(MAC)定位于22例表现为系统性红斑狼疮(SLE)肾炎的肾脏的肾小球和肾小管周围区域。在肾小球中,免疫复合物标志物(IgG、Clq和C3)和MAC的分布相似,尽管与免疫球蛋白和补体成分相比,MAC的沉积物更离散,免疫荧光染色强度更低。相比之下,22例肾脏中只有7例存在肾小管周围免疫复合物,涉及的肾小管簇相对较小,免疫荧光染色比MAC弱,且与间质炎症灶无相关性。在与间质炎症区域相邻的较大肾小管群周边观察到MAC呈颗粒状或不规则线性聚集。在纤维蛋白样坏死区域的血管壁中存在相当数量的IgG、Clq、C3和MAC。这些数据表明,MAC是肾小球、肾小管和血管组织损伤的直接介质。免疫复合物与肾小管周围区域而非肾小球或血管中的MAC之间的不一致性增加了这样一种可能性,即免疫复合物和非免疫因子,如细菌抗原,都可能激活经典或替代补体途径,从而在SLE肾炎肾小管间质病变的发病机制中发挥作用。

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