类风湿关节炎患者外周血多形核中性粒细胞产生补体第三组分(C3)。

C L Yu, C Y Tsai, S C Hsieh, Y Y Tsai, S T Tsai, K H Sun, H S Yu, S H Han
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摘要

经ELISA检测,正常人多形核中性粒细胞(PMN)在体外培养中可自发产生补体第三组分(C3)。tnf - α (20 ng/ml)和细菌脂多糖(100 ng/ml)可增强PMN的c3生成能力,但IL-1 β或IL-8则不能。发现PMN产生C3是温度依赖性的,并被添加蛋白抑制剂抑制。tnf - α或LPS刺激6小时后,通过逆转录辅助聚合酶链反应(RT-PCR)检测PMN中C3 mRNA的表达。为了进一步了解类风湿关节炎(RA)外周血PMN产生C3,我们比较了15例活动性RA、15例非活动性RA和15例正常人外周血PMN自发和tnf - α刺激产生C3的情况。我们没有发现三组之间有任何显著的差异。我们得出结论,PMN在活动性RA患者的C3高补体血症中起着微不足道的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Production of the third component of complement (C3) by peripheral polymorphonuclear neutrophils of the patients with rheumatoid arthritis.

Normal human polymorphonuclear neutrophils (PMN) can spontaneously produce the third component of complement (C3) in in vitro culture as detected by ELISA. This C3-producing capacity of PMN can be augmented by TNF-alpha (20 ng/ml) and bacterial lipopolysaccharide (100 ng/ml), but not by IL-1 beta or IL-8. The C3 production by PMN was found to be temperature dependent and was suppressed by the addition of protein inhibitor. The C3 mRNA in PMN could be detected by reverse transcription assisted polymerase chain reaction (RT-PCR) after TNF-alpha or LPS stimulation for 6 hours. To further understand C3 production by peripheral blood PMN in rheumatoid arthritis (RA), spontaneous and TNF-alpha stimulated production of C3 by peripheral PMN were compared in 15 cases of active RA, 15 inactive RA and 15 normal individuals. We failed to find any significant difference among the three groups. We conclude that PMN plays a negligible role in C3 hypercomplementemia in patients with active RA.

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