In a recent publication featured in the Journal of Inflammation Research, researchers have highlighted that an increase in the expression of C-X-C chemokine receptor 3 (CXCR3) on Vδ2 T cells could potentially enhance their migration into the synovial fluid during gout flare-ups. Additionally, the study suggests that the production of interleukin-17 by these cells might play a part in the development of gout. These discoveries provide valuable insights into potential therapeutic avenues for gout treatment centered around novel strategies involving Vδ2 T cells.
Hong Di and colleagues conducted the study involving 86 patients with gout, 7 with rheumatoid arthritis, 9 with osteoarthritis, and 40 healthy controls. The research revealed that individuals experiencing acute gout displayed significantly lower frequencies of peripheral Vδ2 T cells compared to healthy controls. Moreover, these peripheral Vδ2 T cells exhibited a negative correlation with inflammatory markers. Vδ2 T cells from patients with acute gout tended to accumulate in the synovial fluid, as evidenced by their higher abundance in the synovial fluid compared to serum. Notably, these Vδ2 T cells expressed elevated levels of CXCR3, while the corresponding chemokine, C-X-C motif chemokine ligand 10 (CXCL10), was found at a higher concentration in synovial fluid. Furthermore, Vδ2 T cells derived from the synovial fluid of acute gout patients exhibited increased production of interleukin-17.
Another study by Mo et al. reported that in individuals with rheumatoid arthritis (RA), Vδ2 T cells demonstrate increased chemotactic activity and express higher levels of chemokine receptors, notably C-C chemokine receptor 5 (CCR5) and CXCR3. These elevated levels of chemokine receptors potentially facilitate the migration of Vδ2 T cells into the synovium, thereby contributing to the progression of RA.
The present study reveals that Vδ2 T cells exhibit reduced presence in peripheral blood but accumulate in gout-affected joints during acute phases, with partial recovery during intermittent phases. Moreover, these cells show increased secretion of pro-inflammatory cytokines, particularly IL-17, suggesting their potential involvement in gout pathogenesis. The migration of Vδ2 T cells towards synovial fluid is linked to increased expression of surface CXCR3 and increased levels of its ligand, CXCL10. The study findings not only enhance the knowledge of complex mechanisms of gout but also opens avenues for novel therapeutic strategies targeting Vδ2 T cells in gout treatment.
Reference
- Di H, Han X, Yin Y, Zhang Y, Zeng X. Role of Chemotaxis of Vδ2 T Cells to the Synovium in the Pathogenesis of Acute Gouty Arthritis. J Inflamm Res. 2024;17:721–36.
- Mo WX, Yin SS, Chen H, Zhou C, Zhou JX, Zhao LD, et al. Chemotaxis of Vδ2 T cells to the joints contributes to the pathogenesis of rheumatoid arthritis. Ann Rheum Dis. 2017 Dec;76(12):2075–84.