Differential expression of programmed death 1 (PD-1) on CD4+ and CD8+ T cells in rheumatoid arthritis and psoriatic arthritis

类风湿性关节炎 医学 CD8型 银屑病性关节炎 促炎细胞因子 免疫学 流式细胞术 关节炎 免疫系统 内科学 T细胞 炎症
作者
Joanna Bartosińska,Ewelina Zakrzewska,Anna Król,Dorota Raczkiewicz,Joanna Purkot,Maria Majdan,Dorota Krasowska,Graz̊yna Chodorowska,Krzysztof Giannopoulos
出处
期刊:Polskie Archiwum Medycyny Wewnetrznej-polish Archives of Internal Medicine [Medycyna Praktyczna]
卷期号:127 (12): 815-822 被引量:18
标识
DOI:10.20452/pamw.4137
摘要

INTRODUCTION Rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are characterized by chronic inflammatory processes mediated by proinflammatory cytokines that affect the synovial lining. Programmed death 1 (PD‑1) is a critical regulator of T‑cell activation by downregulating immune responses. OBJECTIVES The aim of the study was to investigate whether the expression of PD‑1 on CD4+ and CD8+ T cells differs between patients with RA and those with PsA. PATIENTS AND METHODS The study included 100 patients with RA, 31 patients with PsA, and 52 healthy controls. The percentages, absolute numbers, and mean fluorescence intensity (MFI) of CD4+PD‑1+ and CD8+PD‑1+T cells from peripheral blood were analyzed using flow cytometry. RESULTS The percentages and absolute numbers of CD4+ and CD8+ T cells with PD‑1 expression were significantly higher in patients with RA than in controls. In patients with PsA, the percentages of CD4+PD‑1+ and CD8+PD‑1+ T cells were significantly lower than in controls. Because of the high frequency of PD-1‑positive T cells in RA and their low frequency in PsA, we analyzed the expression level by analyzing the MFI. The median MFI of PD‑1 on CD4+ and CD8+ T cells was significantly higher in patients with RA (median, 421 and 437, respectively) in comparison with patients with PsA (median, 222 and 198, respectively) and controls (median, 205 and 187, respectively). CONCLUSIONS The differential expression of PD‑1 in RA and PsA suggests that PD‑1 might be involved in autoimmune mechanisms in RA and autoinflammatory mechanisms in PsA in a different manner.

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