RENAL LOCALIZATION OF THE MEMBRANE ATTACK COMPLEX IN SYSTEMIC LUPUS-ERYTHEMATOSUS NEPHRITIS
RENAL LOCALIZATION OF THE MEMBRANE ATTACK COMPLEX IN SYSTEMIC LUPUS-ERYTHEMATOSUS NEPHRITIS
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DOI：
10.1084/jem.154.6.1779
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发表时间：
1981-01-01
影响因子：
15.3
通讯作者：
KOFFLER, D
中科院分区：
文献类型：
--
作者：
BIESECKER, G;KATZ, S;KOFFLER, D
本文报告22例系统性红斑狼疮（SLE）肾炎患者的肾小球及管周均存在补体系统的膜攻击复合物（MAC）。免疫复合物标记物（IgG，补体成分C1q和C3）和MAC在肾小球中观察到类似的分布，尽管MAC沉积物更离散，并且与IG和补体成分相比显示出更低的免疫荧光染色强度。肾小管周围免疫复合物仅存在于22个肾脏中的7个中，涉及相对较小的肾小管簇，表现出比MAC更弱的免疫荧光染色，并且未能与间质性炎症灶相关。在邻近间质性炎症区域的较大肾小管组的外周观察到MAC的颗粒状或不规则线性聚集体。在纤维素样坏死区域的血管壁中存在相当数量的IgG、C1q、C3和MAC。因此，MAC可能是肾小球、肾小管和血管中发生的组织损伤的直接介质。免疫复合物和MAC之间的不一致性定位于肾小管周围区域，但不是在肾小球或血管，提出了免疫复合物和非免疫剂，如细菌抗原，可能激活经典或替代补体途径，从而发挥作用的发病机制中的肾小管间质病变的SLE肾炎。
The membrane attack complex (MAC) of the complement system was localized in glomeruli and peritubular regions of 22 kidneys manifesting systemic lupus erythematosus (SLE) nephritis. A similar distribution was observed for immune complex markers (IgG, complement components C1q and C3) and MAC in glomeruli, although the MAC deposits were more discrete and showed lesser immunofluorescence staining intensity compared with Ig and complement components. Peritubular immune complexes were present in only 7 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, C1q, C3 and MAC were present in blood vessel walls in areas of fibrinoid necrosis. Thus the MAC may be 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.