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豚鼠实验性抗肾小管基底膜肾炎发病机制的研究

Studies on the pathogenesis of experimental anti-tubular basement membrane nephritis in the guinea pig.

作者信息

Van Zwieten M J, Bhan A K, McCluskey R T, Collins A B

出版信息

Am J Pathol. 1976 Jun;83(3):531-46.

PMID:779491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2032497/
Abstract

Using the model of renal disease induced in guinea pigs by immunization with bovine TBM preparations in adjuvant, the following observations were made. Animals with activity induced disease show bright staining for IgG along the TBM and only faint, inconstant staining along the GBM. Following transfer of serum animals with anti-TBM disease to normal recipients, accumulation of IgG was found predominantly in glomeruli at 4 hours, but at Days 3 and 5, IgG was seen predominantly along the TBM. There was no appreciable accumulation of neutrophils in the kidneys of recipients of anti-TBM serum, even at early intervals (4 and 24 hours) after transfer. However, within 2 days, small numbers of mononuclear cells were found. By Day 3, mononuclear cells were numerous, and multinucleate giant cells and tubular cell damage were present. After that, the lesions increased in severity and by 10 days were indistinguishable from those found in actively immunized animals at 14 to 21 days. Study of frozen section of kidneys obtained from animals with active disease at 14 days, employing sheep cells coated with rabbit antibody (IgG EA) revealed rosettes around many of the mononuclear cells in the infiltrate, indicating that they are mononuclear phagocytes (monocytes or macrophages). IgM complexed with sheep cells and complement (EAC) did not react and thus failed to provide evidence for the presence of B lymphocytes. Transfer of 7 X 10(8) lymph node cells from the TBM-immunized Strain 13 donors to normal Strain 13 recipients failed to result in renal lesions. The findings are interpreted as indicating that anti-TBM antibodies mediate the renal disease without the participation of cell-mediated immunity and further that these antibodies bring about an influx of ciculating mononuclear cells, predominantly monocytes, without attracting appreciable numbers of neutrophils.

摘要

利用用佐剂中的牛肾小管基底膜(TBM)制剂免疫豚鼠诱导肾病的模型,进行了以下观察。患有活动性诱导疾病的动物,其肾小管基底膜(TBM)上IgG染色明亮,而肾小球基底膜(GBM)上仅有微弱、不恒定的染色。将患有抗TBM疾病的动物血清转移至正常受体后,4小时时IgG主要在肾小球中积聚,但在第3天和第5天,IgG主要见于肾小管基底膜(TBM)。即使在转移后的早期(4小时和24小时),抗TBM血清受体的肾脏中也没有明显的中性粒细胞积聚。然而,在2天内发现了少量单核细胞。到第3天,单核细胞数量众多,出现了多核巨细胞和肾小管细胞损伤。此后,病变严重程度增加,到第10天时与14至21天主动免疫动物中发现的病变无法区分。对14天时患有活动性疾病的动物肾脏冰冻切片进行研究,使用包被兔抗体(IgG EA)的绵羊细胞,发现浸润中的许多单核细胞周围有玫瑰花结,表明它们是单核吞噬细胞(单核细胞或巨噬细胞)。与绵羊细胞和补体复合的IgM(EAC)没有反应,因此未能提供B淋巴细胞存在的证据。将来自TBM免疫的13号品系供体的7×10⁸个淋巴结细胞转移至正常13号品系受体,未导致肾脏病变。这些发现被解释为表明抗TBM抗体介导了肾脏疾病,而无需细胞介导的免疫参与,并且进一步表明这些抗体导致循环单核细胞,主要是单核细胞的流入,而不吸引大量中性粒细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/dda7f201ec55/amjpathol00451-0124-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/378b88105a35/amjpathol00451-0125-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/5b5c532b1062/amjpathol00451-0125-b.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/46c2c5c5af3d/amjpathol00451-0123-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/ba7f0b6d21bc/amjpathol00451-0124-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/dda7f201ec55/amjpathol00451-0124-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/378b88105a35/amjpathol00451-0125-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/5b5c532b1062/amjpathol00451-0125-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/56702410ce77/amjpathol00451-0126-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/7e06baaa8be6/amjpathol00451-0126-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/46c2c5c5af3d/amjpathol00451-0123-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/ba7f0b6d21bc/amjpathol00451-0124-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb48/2032497/dda7f201ec55/amjpathol00451-0124-b.jpg

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引用本文的文献

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