Abstract

Objective. CD161 has been identified as a marker of human IL-17-producing T cells that are implicated in the pathogenesis of rheumatoid arthritis (RA). This study aimed to investigate the potential link between the percentage of CD161+ T cells and disease activity in RA patients. Methods. Peripheral blood (PB) from 54 RA patients and 21 healthy controls was evaluated. Paired synovial fluid (SF) (n = 17) was analyzed. CD161 expression levels on CD4+, CD8+, and CD4−CD8− T cells were assessed by flow cytometry. Results. The percentage of CD4+CD161+ T cells in RA SF was higher than RA PB, and it was positively correlated with DAS28, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). CD4−CD8−CD161+ T cell percentage was decreased in RA PB and was further reduced in RA SF, and its level in SF was inversely correlated with DAS28, ESR, and CRP. However, CD8+CD161+ T cell percentage was neither changed in RA PB and SF nor correlated with disease activity indices. Conclusion. An increased CD4+CD161+ T cell percentage and a decreased CD4−CD8−CD161+ T cell percentage are present in RA SF and are associated with disease activity, and the accumulation of CD4+CD161+ T cells in SF may contribute to the local inflammation of RA.

Highlights

  • Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by joint inflammation of synovial tissue eventually leading to joint damage and functional disability

  • This study showed that CD4+CD161+ T cells were enriched in synovial fluid (SF), while CD8+CD161+ T cells were not accumulated in SF of RA patients [15]

  • erythrocyte sedimentation rate (ESR) levels tended to be increased in RA patients with collected SF (P = 0.052), and C-reactive protein (CRP) and DAS28 levels were significantly higher in RA patients with collected SF than in total RA patients (P = 0.032 and P = 0.017, resp.)

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Summary

Introduction

Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by joint inflammation of synovial tissue eventually leading to joint damage and functional disability. T helper-type 17 (Th17) cells, a distinct subset of Th cells producing interleukin(IL-) 17 in humans, may be involved in the pathogenesis of autoimmune and chronic inflammatory disorders, including RA [2, 3]. Numerous clinical studies including our data have demonstrated that the percentage of Th17 cells in RA patients was elevated and positively correlated with the degree of local and systemic disease activity [4,5,6]. IL-17A is a proinflammatory cytokine expressed in synovial membrane cultures of RA patients [8] and synovial tissue IL-17 is associated with more rapid joint damage progression in synergy with tumor necrosis factor(TNF-) α [9]. An enhanced expression of IL-17 has been observed in the synovial fluid of RA patients [8, 10], and IL17 has become a new therapeutic target for mouse RA models and human RA [11]

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