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Interleukin-17A Is Produced by CD4+ but Not CD8+ T Cells in Synovial Fluid Following T Cell Receptor Activation and Regulates Different Inflammatory Mediators Compared to Tumor Necrosis Factor in a Model of Psoriatic Arthritis Synovitis.
Arthritis & Rheumatology ( IF 11.4 ) Pub Date : 2020-04-03 , DOI: 10.1002/art.41271
Xiaofei Xu 1 , Nadine Davelaar 1 , Anne-Marie Mus 1 , Patrick S Asmawidjaja 1 , Johanna M W Hazes 1 , Dominique L P Baeten 2 , Marijn Vis 1 , Radjesh J Bisoendial 1 , Errol P Prens 1 , Erik Lubberts 1
Affiliation  

Interleukin‐17A (IL ‐17A) and tumor necrosis factor (TNF ) contribute to the pathogenesis of psoriatic arthritis (PsA). However, their functional relationship in PsA synovitis has not been fully elucidated. Additionally, although CD 8+ T cells in PsA have been recognized via flow cytometry as a source of IL ‐17A production, it is not clear whether CD 8+ T cells secrete IL ‐17A under more physiologically relevant conditions in the context from PsA synovitis. This study was undertaken to clarify the roles of IL ‐17A and TNF in the synovial fluid (SF ) from patients with PsA and investigate the impact of CD 8+ T cells on IL ‐17A production.

中文翻译:

在银屑病关节炎滑膜炎模型中,T细胞受体激活后,滑液中的CD4 + T细胞会产生白细胞介素17A,与肿瘤坏死因子相比,它调节不同的炎症介质。

白介素-17A(IL-17A)和肿瘤坏死因子(TNF)有助于银屑病关节炎(PsA)的发病机理。但是,它们在PsA滑膜炎中的功能关系尚未完全阐明。此外,尽管通过流式细胞仪已将PsA中的CD 8+ T细胞识别为IL-17A产生的来源,但尚不清楚CD 8+ T细胞是否在更生理相关的条件下从PsA滑膜炎中分泌IL -17A。 。这项研究旨在阐明PsA患者滑膜液(SF)中IL-17A和TNF的作用,并研究CD 8+ T细胞对IL-17A产生的影响。
更新日期:2020-04-03
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