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Chemotaxis of Vδ2 T cells to the joints contributes to the pathogenesis of rheumatoid arthritis.

Chemotaxis of Vδ2 T cells to the joints contributes to the pathogenesis of rheumatoid arthritis.
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Mo WX, Yin SS, Chen H, Zhou C, Zhou JX, Zhao LD, Fei YY, Yang HX, Guo JB, Mao YJ, Huang LF, Zheng WJ, Zhang W, Zhang JM, He W, Zhang X,


Mo WX, Yin SS, Chen H, Zhou C, Zhou JX, Zhao LD, Fei YY, Yang HX, Guo JB, Mao YJ, Huang LF, Zheng WJ, Zhang W, Zhang JM, He W, Zhang X, (click to view)

Mo WX, Yin SS, Chen H, Zhou C, Zhou JX, Zhao LD, Fei YY, Yang HX, Guo JB, Mao YJ, Huang LF, Zheng WJ, Zhang W, Zhang JM, He W, Zhang X,

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Annals of the rheumatic diseases 2017 09 0276(12) 2075-2084 doi 10.1136/annrheumdis-2016-211069

Abstract
OBJECTIVES
To explore the role of Vδ2 T cells in the pathogenesis of rheumatoid arthritis (RA).

METHODS
Sixty-eight patients with RA, 21 patients with osteoarthritis and 21 healthy controls were enrolled in the study. All patients with RA fulfilled the 2010 American College of Rheumatology/European League Against Rheumatism criteria for RA. Peripheral Vδ2T population, chemokine receptor expression and proinflammatory cytokine secretion were quantified by flow cytometry. The infiltration of Vδ2 T cells within the synovium was examined by immunohistochemistry and flow cytometry. The effect of tumour necrosis factor (TNF)-α and interleukin (IL)-6 on Vδ2 T migration was determined by flow cytometry and transwell migration assay.

RESULTS
Peripheral Vδ2T cells, but not Vδ1 T cells, were significantly lower in patients with RA, which was negatively correlated with disease activity gauged by Disease Activity Score in 28 joints. Vδ2 T cells from RA accumulated in the synovium and produced high levels of proinflammatory cytokines including interferon-γ and IL-17. Phenotypically, Vδ2 T cells from RA showed elevated chemotaxis potential and expressed high levels of chemokine receptors CCR5 and CXCR3, which was driven by increased serum TNF-α through nuclear factor kappa B signalling. In vivo, TNF-α neutralising therapy dramatically downregulated CCR5 and CXCR3 on Vδ2 T cells and repopulated the peripheral Vδ2 T cells in patients with RA.

CONCLUSIONS
High levels of TNF-α promoted CCR5 and CXCR3 expression in Vδ2 T cells from RA, which potentially infiltrated into the synovium and played crucial roles in the pathogenesis of RA. Targeting Vδ2 T cells might be a potential approach for RA.

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