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银屑病关节炎中的迁移抑制因子

MIG in psoriatic arthritis.

作者信息

Elia G

机构信息

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

出版信息

Clin Ter. 2018 Nov-Dec;169(6):e297-e302. doi: 10.7417/CT.2018.2097.

Abstract

Monokine induced by interferon (IFN)-γ (MIG) / chemokine (C-X-C motif) ligand 9 (CXCL)9 is involved in the pathogenesis of psoriatic arthritis (PsA). It was demonstrated that both blood plasma-derived dendritic cells (pDCs) and pDCs isolated from rheumatoid arthritis (RA) and PsA synovial fluid (SF), expressed CXC receptor (R) 3 and CXCR4, and that the chemotaxis of blood-derived pDCs is stimulated by MIG, (IFN)-γ-inducible protein 10 (IP-10)/CXCL10, IFN-inducible T-cell α chemoattractant (I-TAC) )/CXCL11 and stromal cell-derived factor 1 (SDF-1)/ CXCL12, present in RA and PsA SF. In PsA patients have been found a Th1 immune predominance at early stage of disease, while a reduction of these chemokines has been observed in long lasting PsA, with a significant increase of monocyte chemoattractant protein-1/IP-10 ratio. This suggest a shift from Th1 to the Th2 immune response in long lasting PsA. High levels of MIG has been found in patients with PsA and autoimmune thyroiditis too. This chemokine has been proposed as a useful marker to monitor the activity as well the progression of PsA. Efforts have been made to modulate or prevent the production of MIG in PsA aiming to alter the course of the disease.

摘要

干扰素(IFN)-γ诱导的单核因子(MIG)/趋化因子(C-X-C基序)配体9(CXCL)9参与银屑病关节炎(PsA)的发病机制。研究表明,血浆来源的树突状细胞(pDCs)以及从类风湿关节炎(RA)和PsA滑膜液(SF)中分离出的pDCs均表达CXC受体(R)3和CXCR4,并且RA和PsA滑膜液中存在的MIG、(IFN)-γ诱导蛋白10(IP-10)/CXCL10、IFN诱导的T细胞α趋化因子(I-TAC)/CXCL11和基质细胞衍生因子1(SDF-1)/CXCL12可刺激血液来源的pDCs发生趋化作用。在PsA患者中,疾病早期发现Th1免疫占优势,而在病程较长的PsA患者中观察到这些趋化因子减少,单核细胞趋化蛋白-1/IP-10比值显著增加。这表明病程较长的PsA患者从Th1免疫反应向Th2免疫反应转变。在PsA和自身免疫性甲状腺炎患者中也发现了高水平的MIG。这种趋化因子已被提议作为监测PsA活动及病情进展的有用标志物。人们已努力调节或阻止PsA中MIG的产生,旨在改变疾病进程。

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