Schifferli J A, Taylor R P
Département de Médecine, Hôpital Cantonal Universitaire, Geneva, Switzerland.
Kidney Int. 1989 Apr;35(4):993-1003. doi: 10.1038/ki.1989.83.
Complement participates in the elimination of IC in many circumstances. When antigen/antibody IC first form in the circulation, complement inhibits their aggregation because the covalent binding of C3b to the IC modifies their biophysical properties and they remain soluble. Such opsonized (C3b coated) IC attach to cells bearing C3b receptors (CR1) in the circulation, in particular to erythrocytes, since in humans 85 to 90% of CR1 in the blood is located on these cells. This immune adherence binding reaction appears to be a physiological system that allows IC to be transported through the circulation to the fixed macrophages of the MPS where they are safely eliminated. The deposition of circulating complement-fixing IC in various organs such as the kidney may be considered as a failure of this transport system. This is apparent in complement deficient and depleted states, and also for non-complement-fixing IC (IgA IC). The formation of insoluble IC (by definition immune deposits found in human pathology are insoluble) produces complement activation and inflammation at the site of the immune aggregate.
补体在许多情况下参与免疫复合物（IC）的清除。当抗原/抗体IC首次在循环中形成时，补体抑制它们的聚集，因为C3b与IC的共价结合改变了它们的生物物理特性，使其保持可溶状态。这种被调理（包被有C3b）的IC在循环中附着于带有C3b受体（CR1）的细胞，特别是红细胞，因为在人类中，血液中85%至90%的CR1位于这些细胞上。这种免疫黏附结合反应似乎是一种生理系统，它允许IC通过循环转运至单核吞噬细胞系统（MPS）的固定巨噬细胞处，在那里它们被安全清除。循环中补体结合性IC在诸如肾脏等各种器官中的沉积可被视为该转运系统的失效。这在补体缺陷和耗竭状态下很明显，对于非补体结合性IC（IgA IC）也是如此。不溶性IC的形成（根据定义，在人类病理学中发现的免疫沉积物是不溶性的）会在免疫聚集体部位产生补体激活和炎症反应。
