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关节炎性关节疾病中补体调节蛋白MCP(CD46)、DAF(CD55)和促衰变因子(CD59)的上调。

Upregulation of complement regulators MCP (CD46), DAF (CD55) and protectin (CD59) in arthritic joint disease.

作者信息

Davies M E, Horner A, Loveland B E, McKenzie I F

机构信息

Strangeways Research Laboratory, Worts Causeway, Cambridge, UK.

出版信息

Scand J Rheumatol. 1994;23(6):316-21. doi: 10.3109/03009749409099280.

DOI:10.3109/03009749409099280
PMID:7528443
Abstract

CD46, CD55 and CD59 are cell surface glycoproteins which are widely distributed on normal tissue, where they function in the prevention of complement-mediated damage. In this study we have investigated the altered expression of these molecules under inflammatory conditions both in vitro and in vivo. By using immunocytochemical techniques we demonstrated marked but disparate upregulation of these molecules in IL1-treated cartilage and in diseased cartilage from arthritic joints compared to normal cartilage in both humans and pigs. Expression of these proteins was restricted to the chondrocyte surface, and was also demonstrated on isolated chondrocytes grown in monolayer culture and stimulated with IL1. It is suggested that the elevated levels of these regulatory proteins may be necessary to ameliorate the multiple damaging effects of the inflammatory processes associated with destructive joint diseases.

摘要

CD46、CD55和CD59是细胞表面糖蛋白,广泛分布于正常组织中,在预防补体介导的损伤中发挥作用。在本研究中,我们调查了这些分子在体外和体内炎症条件下的表达变化。通过免疫细胞化学技术,我们证明,与人类和猪的正常软骨相比,在白细胞介素1处理的软骨以及关节炎关节的病变软骨中,这些分子有显著但不同程度的上调。这些蛋白质的表达局限于软骨细胞表面,在单层培养并经白细胞介素1刺激的分离软骨细胞上也得到证实。提示这些调节蛋白水平升高可能是减轻与破坏性关节疾病相关的炎症过程的多种损伤作用所必需的。

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