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银屑病关节炎中γ干扰素诱导的趋化因子

Interferon γ -induced chemokines in psoriatic arthritis.

作者信息

Devito A

机构信息

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

出版信息

Clin Ter. 2014;165(6):e442-6. doi: 10.7417/CT.2014.1790.

DOI:10.7417/CT.2014.1790
PMID:25524203
Abstract

Interferon γ-inducible protein (IP-10) chemokine is implicated in the pathogenesis of psoriatic arthritis (PsA). It was shown that chemokine (C-X-C motif) receptor (CXCR) 3 and CXCR4 were expressed by both blood-derived plasmacytoid dendritic cells (pDCs) and pDCs isolated from rheumatoid arthritis (RA) and PsA synovial fluid (SF) and that IP-10, chemokine (C-X-C motif) ligand (CXCL)-11, and CXCL-12 present in RA and PA SF stimulated chemotaxis of blood-derived pDCs. High circulating levels of IP-10 and chemokine (C-C motif) ligand (CCL) 2 have been found in PsA patients, with a T helper cells (Th) 1 immune predominance in the early phase of the disease. Moreover a decline of IP-10 levels has been observed in long lasting PsA, with a significant increase of the CCL2/IP-10 ratio, suggesting a shift from Th1 to Th2 immune response in long duration PsA. IP-10 levels in PsA patients are significantly higher in presence of autoimmune thyroiditis. IP-10 has been suggested to be a good marker to monitor the activity or progression of PsA. Attempts have been made to modulate or inhibit the production of IP-10 in PsA in order to modify the course of the disease.

摘要

干扰素γ诱导蛋白(IP - 10)趋化因子与银屑病关节炎(PsA)的发病机制有关。研究表明,趋化因子(C - X - C基序)受体(CXCR)3和CXCR4在血液来源的浆细胞样树突状细胞(pDCs)以及从类风湿性关节炎(RA)和PsA滑膜液(SF)中分离出的pDCs中均有表达,并且RA和PA SF中存在的IP - 10、趋化因子(C - X - C基序)配体(CXCL)-11和CXCL - 12可刺激血液来源的pDCs的趋化作用。在PsA患者中发现循环中IP - 10和趋化因子(C - C基序)配体(CCL)2水平较高,在疾病早期以辅助性T细胞(Th)1免疫为主。此外,在病程较长的PsA患者中观察到IP - 10水平下降,CCL2/IP - 10比值显著增加,提示病程较长的PsA患者从Th1免疫反应向Th2免疫反应转变。在合并自身免疫性甲状腺炎的PsA患者中,IP - 10水平显著更高。IP - 10被认为是监测PsA活动或进展的良好标志物。人们已尝试调节或抑制PsA中IP - 10的产生,以改变疾病进程。

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