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类风湿关节炎中肿瘤坏死因子样细胞因子1A(TL1A)及其诱饵受体3(DcR3)的循环水平。

Circulating levels of TNF-like cytokine 1A (TL1A) and its decoy receptor 3 (DcR3) in rheumatoid arthritis.

作者信息

Bamias Giorgos, Siakavellas Spyros I, Stamatelopoulos Kimon S, Chryssochoou Elda, Papamichael Christos, Sfikakis Petros P

机构信息

First Department of Propaedeutic and Internal Medicine, Laikon Hospital, Athens University Medical School, Athens, Greece.

出版信息

Clin Immunol. 2008 Nov;129(2):249-55. doi: 10.1016/j.clim.2008.07.014. Epub 2008 Aug 30.

DOI:10.1016/j.clim.2008.07.014
PMID:18757243
Abstract

TL1A is a novel TNF-like cytokine, which provides co-stimulatory and Th1-polarizing signals to activated lymphocytes, via binding to death-domain receptor 3 (DR3). These functions are inhibited when TL1A associates to decoy receptor 3 (DcR3). We investigated the serum expression of TL1A and DcR3 in 81 patients with RA and 51 healthy controls. TL1A concentrations were elevated in patients by 5-fold (P<0.00001). This increase was more prominent in RFactor-positive patients and correlated with clinical activity in this subgroup. DcR3 was detected more frequently and in significantly higher values in RA-derived sera, correlated strongly with TL1A, and was present in inflammatory synovial fluid. Severe RA stage was associated with highly elevated TL1A and DcR3 serum levels. Treatment with an anti-TNF agent significantly decreased TL1A serum levels. We conclude that TL1A may serve as an inflammatory marker in RA. Interactions between TL1A and its receptors may be important in the pathogenesis of RA.

摘要

TL1A是一种新型的肿瘤坏死因子样细胞因子,它通过与死亡结构域受体3(DR3)结合,为活化的淋巴细胞提供共刺激信号和Th1极化信号。当TL1A与诱饵受体3(DcR3)结合时,这些功能会受到抑制。我们研究了81例类风湿关节炎(RA)患者和51例健康对照者血清中TL1A和DcR3的表达情况。患者血清中TL1A浓度升高了5倍(P<0.00001)。这种升高在类风湿因子(RF)阳性患者中更为显著,并且与该亚组的临床活动相关。在RA患者的血清中,DcR3的检测频率更高,且水平明显更高,与TL1A密切相关,并且存在于炎性滑液中。RA的严重阶段与TL1A和DcR3血清水平的高度升高有关。使用抗TNF药物治疗可显著降低血清中TL1A的水平。我们得出结论,TL1A可能是RA的一种炎症标志物。TL1A与其受体之间的相互作用可能在RA的发病机制中起重要作用。

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