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大鼠被动原位免疫复合物性肾炎发生过程中免疫复合物在肾小球基底膜内的移位

Intraglomerular basement membrane translocation of immune complex (IC) in the development of passive in situ IC nephritis of rats.

作者信息

Fujigaki Y, Nagase M, Honda N

机构信息

First Department of Medicine, Hamamatsu University School of Medicine, Japan.

出版信息

Am J Pathol. 1993 Mar;142(3):831-42.

PMID:8456943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1886793/
Abstract

A study was performed to elucidate the mechanisms of charge-based immune complex nephritis. A chronological observation after induction of nephritis was made by immunoelectron microscopy to clarify whether antigen (Ag) remains in association with antibody (Ab) and C3 during the translocation through the glomerular basement membrane (GBM). Fifteen minutes after intrarenal perfusion with cationized ferritin (pI > 10.0) as Ag, followed by injection of rabbit anti-ferritin Ab, deposition of subendothelial Ag-Ab-C3 complexes was observed. Between 2 hours and 1 day, a large number of Ag in close association with Ab was noted in the lamina densa, but only a small amount of C3 was detectable. During this time Ag and Ab in the subendothelial region gradually decreased. However, C3 reappeared in the subepithelial region together with the Ag-Ab complex after 1 day, and the subendothelial C3 significantly decreased. At 2 hours and day 1, the distributions of Ag and Ab in the GBM were similar in immersion-fixed kidneys regardless of the preperfusion with phosphate-buffered saline. On the other hand, the passage of Ag across the lamina densa was delayed in the experimental rats as compared with the controls. Significant albuminuria also appeared on day 1. Despite the general concept that Ab binding to cationized Ag results in low avidity immune complex, cationized Ag translocated across the GBM in close association with Ab. The complement was activated biphasically in the subendothelial and in the subepithelial space. The subendothelial complement activation may have contributed to the translocation of immune complex.

摘要

进行了一项研究以阐明基于电荷的免疫复合物性肾炎的机制。通过免疫电子显微镜对肾炎诱导后的过程进行了时序观察,以明确抗原(Ag)在通过肾小球基底膜(GBM)转运过程中是否仍与抗体(Ab)和C3结合。以阳离子化铁蛋白(pI > 10.0)作为抗原进行肾内灌注15分钟后,接着注射兔抗铁蛋白抗体,观察到内皮下Ag-Ab-C3复合物的沉积。在2小时至1天之间,在致密层中发现大量与抗体紧密结合的抗原,但仅可检测到少量的C3。在此期间,内皮下区域的抗原和抗体逐渐减少。然而,1天后C3与Ag-Ab复合物一起重新出现在上皮下区域,内皮下的C3显著减少。在2小时和第1天时,无论是否用磷酸盐缓冲盐水预灌注,在浸入固定的肾脏中GBM内抗原和抗体的分布相似。另一方面,与对照组相比,实验大鼠中抗原穿过致密层的过程延迟。在第1天也出现了明显的蛋白尿。尽管一般认为抗体与阳离子化抗原结合会导致低亲和力免疫复合物,但阳离子化抗原与抗体紧密结合穿过GBM。补体在内皮下和上皮下间隙中双相激活。内皮下补体激活可能促进了免疫复合物的转运。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/3ea4492027c2/amjpathol00075-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/16c58b7e712a/amjpathol00075-0172-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/ed1b129147e4/amjpathol00075-0173-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/e3b7d9663395/amjpathol00075-0174-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/99032a6896da/amjpathol00075-0174-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/3ea4492027c2/amjpathol00075-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/16c58b7e712a/amjpathol00075-0172-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/ed1b129147e4/amjpathol00075-0173-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/e3b7d9663395/amjpathol00075-0174-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/99032a6896da/amjpathol00075-0174-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/1886793/3ea4492027c2/amjpathol00075-0175-a.jpg

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A ROLE OF POLYMORPHONUCLEAR LEUKOCYTES AND COMPLEMENT IN NEPHROTOXIC NEPHRITIS.多形核白细胞和补体在肾毒性肾炎中的作用
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