Objective To explore the function and mechanism of CCL19 in the pathogenesis of rheumatoid arthritis. Methods Synovial fibroblasts were collected from 5 cases of rheumatoid arthritis. Peripheral blood mononuclear cells (PBMCs) were obtained from 5 healthy people by Ficoll-Hypaque density gradien centrifugation. The cells were stimulated with IL-1β, TNF-α, IL-17 and other cytokines, and then the expression of CCL19 was detected by RT-PCR. The cells also were treated with different concentration of CCL19, then the expressions of IL-1β, TNF-α were detected by RT-PCR, the expressions of p-ERK, p-p38 were detected by western blot. Results IL-1β promoted the CCL19/CCR7 expression in both synovial fibroblasts and PBMCs. CCL19 upregulated the expression of IL-1β in both synovial fibroblasts and PBMCs. The stimulation of CCL19 also increased its receptor CCR7 expression. CCL19 activated p-ERK and p-p38 in PBMCs. Conclusion The positive feedback loop between CCL19 and IL-1β participate in the development of rheumatoid arthritis.
