Imai H, Chen A, Wyatt R J, Rifai A
Department of Pathology and Laboratory Medicine, University of Texas Health Science Center, Houston.
Clin Exp Immunol. 1988 Sep;73(3):479-83.
Complement activation may play an important role in renal injury associated with glomerular deposition of IgA immune complexes. The ability of naturally occurring human IgA immune complexes (IgA-IC) and covalently cross-linked human IgA oligomers (X-IgA) to activate complement were examined in vitro and in vivo. Large-sized IgA-IC were isolated from a patient's serum by affinity purification (Jacalin-Sepharose) and gel chromatography. Stable X-IgA were prepared by chemical cross-linking with a heterobifunctional reagent, N-succinimdyl 3-(2-pyridyl-dithio) propionate (SPDP). Treatment of fresh normal human serum with large amounts of either IgA-IC or X-IgA failed to activate C3. The C3 consumption was measured immunochemically by the decrease of the B antigen on the native C3 and by the generation of iC3b. Addition of these complexes to serum did not result in cleavage of factor B. Administration of human IgA-IC or X-IgA to mice, killed after 6 h, resulted in glomerular deposition of IgA. Despite the presence of intense glomerular IgA deposits no C3 was detected. Collectively, these findings suggest that neither soluble nor renal localized human IgA complexes activate complement.
补体激活可能在与IgA免疫复合物肾小球沉积相关的肾损伤中起重要作用。在体外和体内研究了天然存在的人IgA免疫复合物（IgA-IC）和共价交联的人IgA寡聚体（X-IgA）激活补体的能力。通过亲和纯化（Jackalin-琼脂糖凝胶）和凝胶色谱从患者血清中分离出大尺寸的IgA-IC。通过与异双功能试剂N-琥珀酰亚胺基3-（2-吡啶基二硫代）丙酸酯（SPDP）化学交联制备稳定的X-IgA。用大量的IgA-IC或X-IgA处理新鲜正常人血清未能激活C3。通过天然C3上B抗原的减少和iC3b的产生免疫化学测量C3消耗。将这些复合物添加到血清中不会导致B因子的裂解。给小鼠注射人IgA-IC或X-IgA，6小时后处死，导致IgA在肾小球沉积。尽管存在强烈的肾小球IgA沉积物，但未检测到C3。总的来说，这些发现表明可溶性或肾局部性人IgA复合物均不能激活补体。
