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巯基乙酸盐刺激的豚鼠腹腔巨噬细胞对补体C1q亚成分的结合及降解增强

Enhanced binding and degradation of the C1q subcomponent of complement by thioglycollate-stimulated guinea pig peritoneal macrophages.

作者信息

Veerhuis R, Klar-Mohamad N, van Es L A, Daha M R

出版信息

Scand J Immunol. 1986 May;23(5):581-7. doi: 10.1111/j.1365-3083.1986.tb01991.x.

DOI:10.1111/j.1365-3083.1986.tb01991.x
PMID:3486466
Abstract

Expression of C1q receptors on the plasma membrane of thioglycollate-stimulated guinea pig peritoneal exudate macrophages increased 1.54 times as compared to unstimulated controls. A Scatchard plot of the binding of 125I-C1q to the cells revealed that the binding is a result of an increase in the number of receptors and not to an increased affinity of the receptors. Thioglycollate-activated macrophages were found to be 1.6 times more active than nonactivated macrophages in the binding of 125I-C1q at 4 degrees C. The enhanced binding of 125I-C1q by activated peritoneal macrophages was reflected in an increase in the amount of 125I-C1q degraded by these cells as compared to resident peritoneal macrophages. This suggests that stimulation of phagocytic cells leads to an increase in the expression of C1q receptors and to a concomitant increase in the uptake and degradation of C1q.

摘要

与未刺激的对照相比,巯基乙酸盐刺激的豚鼠腹腔渗出液巨噬细胞质膜上C1q受体的表达增加了1.54倍。125I-C1q与细胞结合的Scatchard图显示,这种结合是受体数量增加的结果,而不是受体亲和力增加的结果。发现在4℃下,巯基乙酸盐激活的巨噬细胞在结合125I-C1q方面比未激活的巨噬细胞活跃1.6倍。与驻留腹腔巨噬细胞相比,激活的腹腔巨噬细胞对125I-C1q结合的增强反映在这些细胞降解的125I-C1q量的增加上。这表明吞噬细胞的刺激导致C1q受体表达增加,并伴随C1q摄取和降解的增加。

相似文献

1
Enhanced binding and degradation of the C1q subcomponent of complement by thioglycollate-stimulated guinea pig peritoneal macrophages.巯基乙酸盐刺激的豚鼠腹腔巨噬细胞对补体C1q亚成分的结合及降解增强
Scand J Immunol. 1986 May;23(5):581-7. doi: 10.1111/j.1365-3083.1986.tb01991.x.
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Effects of soluble aggregates of IgG on the binding, uptake and degradation of the C1q subcomponent of complement by adherent guinea pig peritoneal macrophages.免疫球蛋白G可溶性聚集体对豚鼠腹膜黏附巨噬细胞结合、摄取和降解补体C1q亚成分的影响。
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The functions of endogenous C1q, a subcomponent of the first component of complement, as a receptor on the membrane of macrophages.内源性C1q(补体第一成分的一个亚成分)作为巨噬细胞膜上的一种受体的功能。
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In vitro modulation of C1q mRNA expression and secretion by interleukin-1, interleukin-6, and interferon-gamma in resident and stimulated murine peritoneal macrophages.白细胞介素-1、白细胞介素-6和干扰素-γ对驻留和受刺激的小鼠腹腔巨噬细胞中C1q mRNA表达及分泌的体外调节作用
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Guinea pig macrophages synthesize a low molecular weight form of C1q with affinity for the C1r2C1s2-complex but which does not bind to Fc in immunoglobulin aggregates.豚鼠巨噬细胞合成一种低分子量形式的C1q,它对C1r2C1s2复合物具有亲和力,但在免疫球蛋白聚集体中不与Fc结合。
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Isolation and characterization of macrophage-derived C1q and its similarities to serum C1q.巨噬细胞源性C1q的分离与鉴定及其与血清C1q的相似性。
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Murine CD93 (C1qRp) contributes to the removal of apoptotic cells in vivo but is not required for C1q-mediated enhancement of phagocytosis.小鼠CD93(C1qRp)有助于体内凋亡细胞的清除,但对于C1q介导的吞噬作用增强并非必需。
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Characterization of C1q by monoclonal antibodies.用单克隆抗体对C1q进行表征。
Behring Inst Mitt. 1984 Nov(76):42-58.

引用本文的文献

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A hierarchical role for classical pathway complement proteins in the clearance of apoptotic cells in vivo.经典途径补体蛋白在体内清除凋亡细胞中的分级作用。
J Exp Med. 2000 Aug 7;192(3):359-66. doi: 10.1084/jem.192.3.359.
2
Serum levels of RHP and of unbound C1q in rheumatoid arthritis and systemic lupus erythematosus.类风湿关节炎和系统性红斑狼疮患者血清中RHP及游离C1q的水平。
Inflammation. 1988 Aug;12(4):351-60. doi: 10.1007/BF00915770.
3
Biosynthesis of normal and low-molecular-mass complement component C1q by cultured human monocytes and macrophages.
培养的人单核细胞和巨噬细胞对正常和低分子量补体成分C1q的生物合成。
Biochem J. 1989 Jan 15;257(2):477-86. doi: 10.1042/bj2570477.
4
Significance of low molecular weight C1q in systemic lupus erythematosus.低分子量C1q在系统性红斑狼疮中的意义。
Ann Rheum Dis. 1990 Sep;49(9):698-704. doi: 10.1136/ard.49.9.698.