Abrass C K, Border W A, Glassock R J
Lab Invest. 1980 Jul;43(1):18-27.
Autologous immune complex nephritis (Heymann nephritis) was actively induced in rats by immunization with high (10 mg.) and low (1 mg.) doses of renal tubular epithelial antigen in complete Freund's adjuvant. The development of proteinuria and granular capillary wall deposition of IgG confirmed the previously well described membranous nephropathy which characterizes this experimental disease. Circulating immune complexes were demonstrated by both the fluid phase and solid phase C1q binding assays in both high and low dose experimental groups. The prevalence of such immune complexes was significantly greater in the experimental than in the control groups immunized with adjuvant alone or liver homogenate in adjuvant. The circulating immune complexes bound to C1q were 16 to 23 S in size and were proven to contain a renal tubular antigen. These data, in combination with the previous demonstration of renal tubular antigen and its antibody in kidneys from rats with autologous immune complex nephritis, are consistent with a circulating immune complex pathogenesis of this model of the actively induced autologous immune complex nephritis in rats.
通过在完全弗氏佐剂中用高剂量（10毫克）和低剂量（1毫克）的肾小管上皮抗原免疫大鼠，主动诱导大鼠发生自体免疫复合物肾炎（海曼肾炎）。蛋白尿的出现以及IgG在毛细血管壁的颗粒状沉积证实了此前已充分描述的膜性肾病，该肾病是这种实验性疾病的特征。在高剂量和低剂量实验组中，通过液相和固相C1q结合试验均证实了循环免疫复合物的存在。与单独用佐剂或佐剂中的肝匀浆免疫的对照组相比，实验中此类免疫复合物的发生率显著更高。与C1q结合的循环免疫复合物大小为16至23 S，并被证明含有肾小管抗原。这些数据，结合之前在患有自体免疫复合物肾炎的大鼠肾脏中证明存在肾小管抗原及其抗体，与大鼠主动诱导的自体免疫复合物肾炎模型的循环免疫复合物发病机制一致。
