Background and aims γδ T cells are important in combating infectious agents and tumour cells. Their role in the pathogenesis of rheumatoid arthritis (RA) remains unknown.
Methods 68 patients with rheumatoid arthritis, 21 patients with osteoarthritis and 21 healthy controls were enrolled in the study. Peripheral Vδ2T population, apoptosis, proliferation, chemokine receptor expression and pro-inflammatory cytokine secretion were quantified by flow cytometry. The infiltration of Vδ2 T cells within synovium was examined by immunohistochemistry and flow cytometry. The effect of TNF-α and IL-6 on Vδ2 T migration was determined by flow cytometry and trans-well migration assay.
Results The percentage of peripheral Vδ2T cells of active RA were significantly decreased compared with healthy controls, which were negatively correlated with the disease activity indexes including DAS28, CRP and ESR. However, the Vδ2T cells infiltrated in the synovium of RA were increased compared with OA (p<0.05). Comparing with OA Vδ2T cells, both peripheral and synovium Vδ2T cells of RA produced higher level of IFN-γ and IL-17 (p<0.05). The chemokine receptor CCR5 and CXCR3 expressed on Vδ2T cells in RA were significantly higher than HC and OA patients (p<0.05), which were induced by TNF-α and IL-6. TNF-α antagonist therapy restored the peripheral Vδ2 T cell in RA.
Conclusions Elevated TNF-α in RA patients induced high expression of CCR5 and CXCR3 on Vδ2T cells, which subsequently promote Vδ2 T cells infiltrate into synovium and play an important role in the pathogenesis of RA. Vδ2 T cell is a promising potential biomarker and therapeutic target of RA.
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