Yamamoto K, Oite T, Kihara I, Shimizu F
Clin Exp Immunol. 1984 Sep;57(3):575-82.
Experimental immune complex glomerulonephritis was induced with human IgG (HIgG) in two strains of rats, Wistar-King-Aptekman (WKA) and spontaneously hypertensive rats (SHR). The rats were pre-immunized s.c. with 1 mg of HIgG in Freund's complete adjuvant, and 8 weeks later were given a daily i.v. 2 mg of HIgG injections for 4 weeks. Renal tissue, obtained at weekly intervals after the beginning of i.v. injections, was examined by light, immunofluorescence and electron microscopic tests. SHR developed an endocapillary proliferative glomerulonephritis with heavy proteinuria after the administration of HIgG for 4 weeks. They had massive depositions of HIgG, rat IgG, and rat C3 both in the mesangial area and along the capillary wall. On the other hand, in WKA rats, the proliferative lesions were scarcely seen and the immune deposits were observed almost exclusively in the mesangium. Moreover, urinary protein excretion of these rats was within normal range. In comparison with bovine serum albumin (BSA) nephritis in SHR, HIgG-induced glomerular lesion was relatively mild. This difference seemed attributable to the nature of the HIgG, such as its molecular weight and immunogenicity.
用人类免疫球蛋白(HIgG)在两种品系的大鼠,即Wistar-King-Aptekman(WKA)大鼠和自发性高血压大鼠(SHR)中诱导实验性免疫复合物肾小球肾炎。大鼠皮下预先用1mg HIgG与弗氏完全佐剂免疫,8周后每天静脉注射2mg HIgG,共注射4周。在静脉注射开始后每周间隔获取肾组织,通过光镜、免疫荧光和电子显微镜检查。SHR在给予HIgG 4周后发生毛细血管内增生性肾小球肾炎并伴有大量蛋白尿。它们在系膜区和沿毛细血管壁均有大量HIgG、大鼠IgG和大鼠C3沉积。另一方面,在WKA大鼠中,几乎未见增生性病变,免疫沉积物几乎仅见于系膜区。此外,这些大鼠的尿蛋白排泄在正常范围内。与SHR中的牛血清白蛋白(BSA)肾炎相比,HIgG诱导的肾小球病变相对较轻。这种差异似乎归因于HIgG的性质,如分子量和免疫原性。