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通过静脉注射异种抗大鼠肾小管抗体诱导大鼠自体免疫复合物性肾小球肾炎。II. 早期肾小球病变

Induction of an autologous immune complex glomerulonephritis in the rat by intravenous injection of heterologous anti-rat kidney tubular antibody. II. Early glomerular lesions.

作者信息

Barabas A Z, Lannigan R

出版信息

Br J Exp Pathol. 1974 Jun;55(3):282-90.

PMID:4278533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2072638/
Abstract

The early effects of a single intravenous injection of anti-rat kidney tubular fraction 3 antibody were studied in rats pretreated with BSA and in untreated animals. Definite deposition of immune complexes, which stained for rat IgG, were noted in the glomeruli of the BSA pretreated rats after one day and in the untreated rats by the fourth day with the fluorescent antibody technique. Control animals injected with normal rabbit serum or BSA and normal controls did not develop immune complex glomerulonephritis. Two of the 4 surviving rats pretreated with BSA and injected with the anti-tubular fraction 3 antibody developed proteinuria towards the fourth week, whereas proteinuria did not occur in the untreated and the control rats. It is possible that the heterologous anti-rat kidney tubular fraction 3 antibody releases a nephritogenic antigen from the proximal convoluted tubules soon after its administration. Autoantibodies formed are presumably able to form immune complexes with the nephritogenic antigen and produce glomerular injury. As a result of the glomerular damage, the autoantibodies may gain access to the proximal convoluted tubular cells and maintain the release of the nephritogenic antigen. The developing kidney disease is morphologically similar in every respect to autologous immune complex glomerulonephritis.

摘要

在预先用牛血清白蛋白(BSA)处理的大鼠和未处理的动物中,研究了单次静脉注射抗大鼠肾小管3组分抗体的早期效应。采用荧光抗体技术,在预先用BSA处理的大鼠肾小球中,一天后就观察到了明确的免疫复合物沉积,这些复合物对大鼠IgG呈阳性染色;在未处理的大鼠中,到第四天时也观察到了这种沉积。注射正常兔血清或BSA的对照动物以及正常对照组均未发生免疫复合物性肾小球肾炎。4只预先用BSA处理并注射抗肾小管3组分抗体的存活大鼠中,有2只在第四周左右出现蛋白尿,而未处理的大鼠和对照大鼠未出现蛋白尿。有可能异源性抗大鼠肾小管3组分抗体在给药后不久就从近端曲管释放出一种致肾炎抗原。形成的自身抗体大概能够与致肾炎抗原形成免疫复合物并造成肾小球损伤。由于肾小球损伤,自身抗体可能进入近端曲管细胞并维持致肾炎抗原的释放。所发生的肾脏疾病在形态学上与自身免疫复合物性肾小球肾炎在各方面都相似。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/19728f7c1100/brjexppathol00405-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/407b08615dab/brjexppathol00405-0100-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/4c6171f04cef/brjexppathol00405-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/4ebf266fe1ec/brjexppathol00405-0098-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/445547af8028/brjexppathol00405-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/fd76d48d721e/brjexppathol00405-0096-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/19728f7c1100/brjexppathol00405-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/407b08615dab/brjexppathol00405-0100-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/4c6171f04cef/brjexppathol00405-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/4ebf266fe1ec/brjexppathol00405-0098-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/445547af8028/brjexppathol00405-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/fd76d48d721e/brjexppathol00405-0096-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e64/2072638/19728f7c1100/brjexppathol00405-0099-a.jpg

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本文引用的文献

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Production of nephrotic syndrome in rats by Freund's adjuvants and rat kidney suspensions.用弗氏佐剂和大鼠肾悬液在大鼠中诱发肾病综合征
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Chemotaxis of polymorphs induced by tissue antigens and normal serum in rats: a possible clearance mechanism.大鼠体内组织抗原和正常血清诱导的多形核白细胞趋化作用:一种可能的清除机制。
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Passive Heymann nephritis in the rat produced by a heterologous antibody to a heterologous kidney fraction 3 antigen.由针对异种肾部分3抗原的异种抗体在大鼠中产生的被动海曼肾炎。
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Stimulation of circulating autoantibody levels in the rat with established progressive passive Heymann nephritis.用已建立的进行性被动海曼肾炎刺激大鼠循环自身抗体水平。
Clin Exp Immunol. 1986 Jul;65(1):34-41.
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Br J Exp Pathol. 1976 Oct;57(5):555-9.
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与亚细胞器官抗原发生反应的体液抗体的致病作用研究。II. 用抗大鼠兔免疫血清对大鼠进行被动免疫。
Immunology. 1967 Apr;12(4):389-94.
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The immune response after tissue injury.
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8
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