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末端补体复合物可能参与活动性海曼肾炎。

Possible involvement of terminal complement complex in active Heymann nephritis.

作者信息

de Heer E, Daha M R, Bhakdi S, Bazin H, van Es L A

出版信息

Kidney Int. 1985 Feb;27(2):388-93. doi: 10.1038/ki.1985.21.

DOI:10.1038/ki.1985.21
PMID:3886996
Abstract

We investigated whether the appearance of various complement components in renal deposits of immune complexes correlated with the development of proteinuria in rats with active Heymann nephritis. Sequential kidney biopsy specimens and serum samples were obtained from Lewis rats immunized with Fx1A in complete Freund's adjuvant. Circulating antibodies against purified auto-antigen renal tubular epithelial glycoprotein, as measured by ELISA, were found in the circulation together with a diffuse granular deposition of IgG1, IgG2a, and IgG2b in the glomeruli within 2 weeks after immunization. Biopsy specimens taken 4 weeks after immunization showed diffuse deposition of C4 and C3, which indicated that activation of complement by the classical pathway had occurred. The detection of the C5b-9 complex of complement in glomerular deposits coincided with the development of abnormal proteinuria indicating that the glomerular damage in this autoimmune disease may be caused by complement-mediated lesions in the glomerular capillary walls.

摘要

我们研究了免疫复合物肾沉积物中各种补体成分的出现是否与活动性海曼肾炎大鼠蛋白尿的发生相关。从用弗氏完全佐剂中的Fx1A免疫的Lewis大鼠获取连续的肾脏活检标本和血清样本。免疫后2周内,通过ELISA检测发现循环中存在针对纯化的自身抗原肾小管上皮糖蛋白的循环抗体,同时肾小球内有IgG1、IgG2a和IgG2b的弥漫性颗粒沉积。免疫后4周采集的活检标本显示C4和C3弥漫性沉积,这表明经典途径的补体激活已经发生。肾小球沉积物中补体C5b - 9复合物的检测与异常蛋白尿的发生同时出现,表明这种自身免疫性疾病中的肾小球损伤可能是由肾小球毛细血管壁中补体介导的病变引起的。

相似文献

1
Possible involvement of terminal complement complex in active Heymann nephritis.末端补体复合物可能参与活动性海曼肾炎。
Kidney Int. 1985 Feb;27(2):388-93. doi: 10.1038/ki.1985.21.
2
Antibodies to glycolipids activate complement and promote proteinuria in passive Heymann nephritis.抗糖脂抗体激活补体并促进被动型海曼肾炎中的蛋白尿。
Am J Pathol. 1994 Apr;144(4):807-19.
3
Influence of renal transplantation in rats on glomerular and tubular immune complexes.大鼠肾移植对肾小球和肾小管免疫复合物的影响。
Am J Kidney Dis. 1986 Jan;7(1):69-75. doi: 10.1016/s0272-6386(86)80058-0.
4
Increased urinary excretion of C5b-9 distinguishes passive Heymann nephritis in the rat.C5b - 9尿排泄增加可区分大鼠被动型海曼肾炎。
Kidney Int. 1989 Jan;35(1):60-8. doi: 10.1038/ki.1989.8.
5
Detection of terminal complement components in experimental immune glomerular injury.实验性免疫性肾小球损伤中终末补体成分的检测
Kidney Int. 1984 Dec;26(6):830-7. doi: 10.1038/ki.1984.225.
6
Urinary excretion of C5b-9 reflects disease activity in passive Heymann nephritis.C5b - 9的尿排泄反映了被动型海曼肾炎的疾病活动情况。
Kidney Int. 1989 Jul;36(1):65-71. doi: 10.1038/ki.1989.162.
7
Passive Heymann nephritis with acute and severe proteinuria induced by heterologous antibody against renal tubular brush border glycoprotein gp108.由抗肾小管刷状缘糖蛋白gp108的异源抗体诱导的伴有急性和严重蛋白尿的被动性海曼肾炎。
Lab Invest. 1986 Jul;55(1):63-70.
8
Analysis of glomeruli-eluted Gp330 autoantibodies and of Gp330 antigen of Heymann nephritis.对肾小球洗脱的Gp330自身抗体及海曼肾炎的Gp330抗原的分析。
J Immunol. 1993 Dec 1;151(11):6500-8.
9
Inhibition of complement regulation is key to the pathogenesis of active Heymann nephritis.补体调节的抑制是活动性海曼肾炎发病机制的关键。
J Exp Med. 1998 Oct 5;188(7):1353-8. doi: 10.1084/jem.188.7.1353.
10
Complement and monocytes are essential for provoking glomerular injury in passive Heymann nephritis in rats. Terminal complement components are not the sole mediators of proteinuria.补体和单核细胞对于引发大鼠被动性海曼肾炎中的肾小球损伤至关重要。补体终末成分并非蛋白尿的唯一介质。
Lab Invest. 1991 Aug;65(2):168-79.

引用本文的文献

1
Specific increases in urinary excretion of anti-DNA antibodies in lupus mice induced by lysozyme administration: further evidence for DNA-anti-DNA immune complexes in the pathogenesis of nephritis.溶菌酶给药诱导的狼疮小鼠抗DNA抗体尿排泄量特异性增加:肾炎发病机制中DNA - 抗DNA免疫复合物的进一步证据。
Clin Exp Immunol. 1993 Jan;91(1):115-20. doi: 10.1111/j.1365-2249.1993.tb03364.x.
2
Heymann nephritis revisited--new insights into the pathogenesis of experimental membranous glomerulonephritis.重温海曼肾炎——对实验性膜性肾小球肾炎发病机制的新见解
Clin Exp Immunol. 1993 Dec;94(3):393-4.
3
Epitope specificity of anti-gp330 autoantibodies determines the development of proteinuria in active Heymann nephritis.
抗gp330自身抗体的表位特异性决定了活动性海曼肾炎中蛋白尿的发展。
Am J Pathol. 1993 Mar;142(3):821-9.
4
Circulatory antigen of Heymann nephritis. II. Isolation of a 70,000 MW antigen from normal rat serum which cross-reacts with Heymann nephritis antigen.海曼肾炎的循环抗原。II. 从正常大鼠血清中分离出一种分子量为70,000的抗原,它与海曼肾炎抗原发生交叉反应。
Immunology. 1986 Nov;59(3):451-8.
5
Complement-induced glomerular epithelial cell injury. Role of the membrane attack complex in rat membranous nephropathy.补体诱导的肾小球上皮细胞损伤。膜攻击复合物在大鼠膜性肾病中的作用。
J Clin Invest. 1986 Apr;77(4):1096-107. doi: 10.1172/JCI112408.
6
Cyclosporin A induces long-term unresponsiveness in mercuric chloride-induced autoimmune glomerulonephritis.环孢素A可诱导氯化汞所致自身免疫性肾小球肾炎的长期无反应性。
Clin Exp Immunol. 1988 Aug;73(2):307-11.
7
Complement membrane attack complex stimulates production of reactive oxygen metabolites by cultured rat mesangial cells.补体膜攻击复合物刺激培养的大鼠系膜细胞产生活性氧代谢产物。
J Clin Invest. 1986 Mar;77(3):762-7. doi: 10.1172/JCI112372.
8
Molecular cloning of S-protein, a link between complement, coagulation and cell-substrate adhesion.S蛋白的分子克隆,补体、凝血与细胞-底物黏附之间的联系
EMBO J. 1985 Dec 1;4(12):3153-7. doi: 10.1002/j.1460-2075.1985.tb04058.x.
9
Complement membrane attack on nucleated cells: resistance, recovery and non-lethal effects.补体对有核细胞的膜攻击:抗性、恢复及非致死效应。
Biochem J. 1989 Nov 15;264(1):1-14. doi: 10.1042/bj2640001.
10
Depletion of C6 prevents development of proteinuria in experimental membranous nephropathy in rats.C6的缺失可预防大鼠实验性膜性肾病中蛋白尿的发生。
Am J Pathol. 1989 Jul;135(1):185-94.