Sado Y, Naito I, Okigaki T
Division of Immunology, Shigei Medical Research Institute, Okayama, Japan.
J Pathol. 1989 Aug;158(4):325-32. doi: 10.1002/path.1711580410.
Anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM nephritis) was transferred from nephritic rats to normal recipient rats with isologous antibodies obtained from the urine of the nephritic rats. The original actively-immunized anti-GBM nephritis was induced in inbred WKY/NCrj rats by injecting the nephritogenic antigen from bovine renal basement membranes. Excreted urinary antibodies were collected, purified, and then injected into recipient rats of the same strain. Haematuria and proteinuria appeared on day 2 and day 3, respectively; both became heavier and reached a plateau by day 5. Endocapillary hypercellularity of mononuclear cells in glomeruli was the first histological change, which was observed from day 2, and later extracapillary changes such as fibrin deposition, capsular adhesion, and crescent formation were observed. These histological changes were the same as those seen in the actively-immunized nephritis. The results demonstrate that anti-GBM nephritis is clearly induced by autoantibodies. This new passively-immunized model of anti-GBM nephritis makes it possible and easier to analyse further the mechanism of anti-GBM nephritis because only isologous antibodies are used. This study also indicates that the urine of the nephritic rat is a good source of autoantibodies.
抗肾小球基底膜抗体诱导的肾小球肾炎（抗GBM肾炎）通过将从患肾炎大鼠尿液中获得的同种抗体从患肾炎大鼠转移至正常受体大鼠而得以实现。最初的主动免疫性抗GBM肾炎是通过向近交系WKY/NCrj大鼠注射来自牛肾基底膜的致肾炎抗原诱导产生的。收集、纯化排泄的尿液抗体，然后将其注射到同一品系的受体大鼠体内。血尿和蛋白尿分别在第2天和第3天出现；两者均加重，并在第5天达到平台期。肾小球内单核细胞的毛细血管内细胞增多是最早观察到的组织学变化，在第2天即可观察到，随后观察到毛细血管外变化，如纤维蛋白沉积、包膜粘连和新月体形成。这些组织学变化与主动免疫性肾炎中所见的变化相同。结果表明，抗GBM肾炎显然是由自身抗体诱导的。这种新的抗GBM肾炎被动免疫模型使得进一步分析抗GBM肾炎的机制变得可行且更容易，因为仅使用了同种抗体。本研究还表明，患肾炎大鼠的尿液是自身抗体的良好来源。
