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CXCR6-CXCL16 interaction in the pathogenesis of Juvenile Idiopathic Arthritis.

机译:CXCR6-CXCL16相互作用在青少年特发性关节炎的发病机理中。

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In order to evaluate the role of CXCR6/CXCL16 in driving lymphocyte migration into inflamed joints of children with oligoarticular Juvenile Idiopathic Arthritis (JIA) we analysed CXCR6 expression and functional capability in lymphocytes from synovial fluid (SF) by flow cytometry, by real-time polymerase chain reaction (RT-PCR) and migration assays. Furthermore, CXCR6 and CXCL16 expression in synovial tissue (ST) was analysed by immunohistochemistry. T cells isolated from SF of patients with JIA expressed CXCR6 which was functionally active as shown by chemotactic assays. The same cells expressed CXCR3 and it exerted a migratory activity in response to CXCL10. CXCL16 and CXCR6 were intensively expressed on the synovium cells, respectively on macrophages, synoviocytes and endothelial cells and on lymphocytes, synoviocytes and endothelial cells. Taken together, these data suggest that CXCR6 and CXCR3 act coordinately with respective ligands and are involved in the pathophysiology of JIA-associated inflammatory processes.
机译:为了评估CXCR6 / CXCL16在驱动淋巴细胞迁移至少关节性特发性关节炎(JIA)儿童发炎关节中的作用,我们通过流式细胞术,实时分析了滑液(SF)淋巴细胞中CXCR6的表达和功能能力。聚合酶链反应(RT-PCR)和迁移分析。此外,通过免疫组织化学分析了滑膜组织(ST)中CXCR6和CXCL16的表达。从JIA患者的SF中分离出的T细胞表达了CXCR6,其功能如趋化分析所示。相同的细胞表达CXCR3,并响应CXCL10发挥迁移活性。 CXCL16和CXCR6在滑膜细胞上分别在巨噬细胞,滑膜细胞和内皮细胞上以及在淋巴细胞,滑膜细胞和内皮细胞上强烈表达。综上所述,这些数据表明CXCR6和CXCR3与各自的配体协同作用,并参与JIA相关的炎症过程的病理生理。

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