Feehally J, Beattie T J, Brenchley P E, Coupes B M, Mallick N P, Postlethwaite R J
Kidney Int. 1986 Dec;30(6):924-31. doi: 10.1038/ki.1986.274.
Cellular and immunochemical parameters of the IgA system were studied in 15 subjects with IgA nephropathy (IgAN) and 15 agematched controls. In IgAN remission no abnormalities of the IgA system were detectable by the methods used. In IgAN relapse, [macroscopic hematuria associated with upper respiratory tract infection (URTI) (N = 6)] there were rises in IgA-bearing B-lymphocytes (three of six), T helper/suppressor cell ratio (six of six) and pokeweed mitogen-induced IgA production (four of six). Total serum and salivary IgA were unchanged. Serum IgA profile (HPLC-ELISA) showed increases in polymer IgA (three of six). No such changes were found during URTI in controls. These findings support the view that an exaggerated IgA response to mucosal antigen challenge initiates glomerular damage and hematuria in IgAN.
对15例IgA肾病（IgAN）患者和15例年龄匹配的对照者的IgA系统的细胞和免疫化学参数进行了研究。在IgAN缓解期，所采用的方法未检测到IgA系统异常。在IgAN复发期，[与上呼吸道感染（URTI）相关的肉眼血尿（N = 6）]，携带IgA的B淋巴细胞增加（6例中的3例），辅助性T细胞/抑制性T细胞比值升高（6例中的6例），商陆有丝分裂原诱导的IgA产生增加（6例中的4例）。血清和唾液总IgA无变化。血清IgA谱（HPLC-ELISA）显示聚合IgA增加（6例中的3例）。对照组在URTI期间未发现此类变化。这些发现支持这样的观点，即对黏膜抗原刺激的过度IgA反应引发了IgAN中的肾小球损伤和血尿。
