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急性血清病中的补体固定:肾小球结合的C3转化酶的组装。

Complement fixation in acute serum sickness: assembly of glomerular-bound C3-convertase.

作者信息

Bartolotti S R, Peters D K

出版信息

Clin Exp Immunol. 1979 Sep;37(3):391-8.

PMID:389495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1537795/
Abstract

Complement (C) fixing properties of glomerular immune deposits were studied in vitro in two groups of rabbits with acute serum sickness (ASS). Deposits were studied early in decomplemented (cobra venom factor-treated) rabbits (Group I) and during the evolution of the nephritis in non-decomplemented rabbits (Group II). Following perfusion of kidneys of animals from Group I (which contained no autologous C3) with rabbit serum deficient in factor B (classical pathway) or serum pre-treated with Mg++EGTA (alternative pathway), fixation of C3 was observed in both systems. No C3 deposition was found when EDTA-rabbit serum was used. When kidney sections obtained from serial biopsies and autopsy material from Group II (which contained rabbit C3-C3rb) were incubated with purified factors B and D, followed by either purified human C3 (C3hu) or EDTA-guinea-pig serum (C3gp), fixation of C3hu or C3gp to early C3 deposits was observed. When sections were pre-incubated with heat-inactivated rabbit serum (source of C3b-inactivator), C3 fixation was substantially reduced. Little or no C3 fixation was found after incubation of sections with human or guinea-pig serum depleted of factor D (classical pathway). Thus, in ASS, glomerular complement deposition appears to be predominantly dependent on the activation of the alternative pathway (C3b-feedback) which is progressively lost during the evolution of the nephritis.

摘要

在两组患有急性血清病(ASS)的兔子中,对肾小球免疫沉积物的补体(C)固定特性进行了体外研究。在补体缺失(用眼镜蛇毒因子处理)的兔子(第一组)早期研究沉积物,在未补体缺失的兔子(第二组)肾炎发展过程中研究沉积物。用缺乏B因子的兔血清(经典途径)或用Mg++EGTA预处理的血清(替代途径)灌注第一组动物(不含自体C3)的肾脏后,在两个系统中均观察到C3的固定。当使用EDTA - 兔血清时,未发现C3沉积。当将从第二组(含有兔C3 - C3rb)的系列活检和尸检材料获得的肾脏切片与纯化的B因子和D因子孵育,然后用纯化的人C3(C3hu)或EDTA - 豚鼠血清(C3gp)孵育时,观察到C3hu或C3gp固定到早期C3沉积物上。当切片预先用热灭活的兔血清(C3b灭活剂来源)孵育时,C3固定显著减少。在用缺乏D因子的人或豚鼠血清(经典途径)孵育切片后,几乎没有或没有发现C3固定。因此,在急性血清病中,肾小球补体沉积似乎主要依赖于替代途径(C3b反馈)的激活,而该途径在肾炎发展过程中逐渐丧失。

相似文献

1
Complement fixation in acute serum sickness: assembly of glomerular-bound C3-convertase.急性血清病中的补体固定:肾小球结合的C3转化酶的组装。
Clin Exp Immunol. 1979 Sep;37(3):391-8.
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Delayed removal of renal-bound antigen in decomplemented rabbits with acute serum sickness.补体缺乏的急性血清病兔体内肾结合抗原的延迟清除
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引用本文的文献

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Curcumin alleviates immune-complex-mediated glomerulonephritis in factor-H-deficient mice.姜黄素减轻补体因子 H 缺陷型小鼠免疫复合物介导的肾小球肾炎。
Immunology. 2013 Jul;139(3):328-37. doi: 10.1111/imm.12079.
2
Chronic serum sickness glomerulonephritis: removal of glomerular antigen and electron-dense deposits is largely dependent on plasma complement.慢性血清病性肾小球肾炎:肾小球抗原和电子致密沉积物的清除很大程度上依赖于血浆补体。
Clin Exp Immunol. 1988 Oct;74(1):126-30.
3
Stimulation of mesangial phagocytes does not influence the removal of established glomerular immune complex deposits.对系膜吞噬细胞的刺激并不影响已形成的肾小球免疫复合物沉积物的清除。
Int J Exp Pathol. 1990 Aug;71(4):529-36.

本文引用的文献

1
Quantitative estimation of proteins by electrophoresis in agarose gel containing antibodies.在含有抗体的琼脂糖凝胶中通过电泳对蛋白质进行定量估计。
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Antigen quantitation in experimental immune complex glomerulonephritis. I. Acute serum sickness.实验性免疫复合物性肾小球肾炎中的抗原定量。I. 急性血清病
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A method of trace iodination of proteins for immunologic studies.一种用于免疫学研究的蛋白质微量碘化方法。
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7
The C3-activator system: an alternate pathway of complement activation.C3激活剂系统:补体激活的替代途径。
J Exp Med. 1971 Sep 1;134(3 Pt 2):90s-108s.
8
Requirements for the solubilization of immune aggregates by complement: assembly of a factor B-dependent C3-convertase on the immune complexes.补体溶解免疫聚集体的条件:免疫复合物上B因子依赖性C3转化酶的组装。
J Exp Med. 1977 Jan 1;145(1):86-100. doi: 10.1084/jem.145.1.86.
9
Haemolytic diffusion plate assays for factors B and D of the alternative pathway of complement activation.补体激活替代途径中B因子和D因子的溶血扩散平板试验。
Immunochemistry. 1976 Apr;13(4):317-24. doi: 10.1016/0019-2791(76)90341-4.
10
In vitro fixation of guinea pig complement by renal biopsies.肾活检对豚鼠补体的体外固定作用
J Clin Lab Immunol. 1979 Feb;1(4):299-304.