Background: This study aimed to explore the potential roles of Vδ 2 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 Vδ 2 T cells was determined by transwell migration assay. The levels of chemokines were also detected by enzyme-linked immunosorbent assay.
Results: Peripheral Vδ 2 T cells had significantly lower frequencies in acute gout patients than that in healthy controls (P< 0.001). These peripheral Vδ 2 T cells were negatively correlated with inflammatory markers. Vδ 2 T cells from acute gout patients accumulated in synovial fluid, as evidenced by a higher abundance of Vδ 2 T cells in it than that in the serum (P< 0.01). And Vδ 2 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). Vδ 2 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 Vδ 2 T cells potentially facilitates their infiltration into synovial fluid during acute gouty arthritis. Further production of interleukin-17 by Vδ 2 T cells may contribute to the pathogenesis of gout. This study sheds new light on developing novel Vδ 2 T cells-based therapeutic strategies for gout treatment.

Keywords: acute gouty arthritis, γδT cells, Vδ 2 T cells, Interleukin-17, CXCR3, CXCL10