Role of Chemotaxis of Vδ2 T Cells to the Synovium in the Pathogenesis of Acute Gouty Arthritis

Abstract

Background This study aimed to explore the potential roles of Vδ2 T cells in the pathogenesis of acute gouty arthritis. Methods Patients with gout (n=86), rheumatoid arthritis (n=7), osteoarthritis (n=9), and healthy controls (n=40) were enrolled. γδT cell frequency, chemokine receptor expression and production of pro-inflammatory cytokines in cells from peripheral blood and synovial fluid samples were quantified by flow cytometry. The chemotaxis ability of Vδ2 T cells was determined by transwell migration assay. The levels of chemokines were also detected by enzyme-linked immunosorbent assay. Results Peripheral Vδ2 T cells had significantly lower frequencies in acute gout patients than that in healthy controls ( P <0.001). These peripheral Vδ2 T cells were negatively correlated with inflammatory markers. Vδ2 T cells from acute gout patients accumulated in synovial fluid, as evidenced by a higher abundance of Vδ2 T cells in it than that in the serum ( P <0.01). And Vδ2 T cells expressed a high level of C-X-C chemokine receptor 3 ( P =0.035), and its corresponding chemokine C-X-C motif chemokine ligand 10 showed a high concentration in synovial fluid ( P <0.05). Vδ2 T cells from synovial fluid of acute gout patients produced a high level of interleukin-17 ( P =0.033). Conclusion The up-regulated expression of C-X-C chemokine receptor 3 on Vδ2 T cells potentially facilitates their infiltration into synovial fluid during acute gouty arthritis. Further production of interleukin-17 by Vδ2 T cells may contribute to the pathogenesis of gout. This study sheds new light on developing novel Vδ2 T cells-based therapeutic strategies for gout treatment.