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Effect of JAK Inhibition on the Induction of Proinflammatory HLA–DR+CD90+ Rheumatoid Arthritis Synovial Fibroblasts by Interferon-γ
Arthritis & Rheumatology ( IF 13.3 ) Pub Date : 2021-08-25 , DOI: 10.1002/art.41958
Shuyang Zhao 1 , Ricardo Grieshaber-Bouyer 2 , Deepak A Rao 3 , Philipp Kolb 4 , Haizhang Chen 4 , Ivana Andreeva 1 , Theresa Tretter 1 , Hanns-Martin Lorenz 1 , Carsten Watzl 5 , Guido Wabnitz 1 , Lars-Oliver Tykocinski 1 , Wolfgang Merkt 6
Affiliation  

Findings from recent transcriptome analyses of the synovium of patients with rheumatoid arthritis (RA) have revealed that 15-fold expanded HLA–DR+CD90+ synovial fibroblasts potentially act as key mediators of inflammation. The reasons for the expansion of HLA–DR+CD90+ synovial fibroblasts are unclear, but genetic signatures indicate that interferon-γ (IFNγ) plays a central role in the generation of this fibroblast subset. The present study was undertaken to investigate the generation, function and therapeutically intended blockage of HLA–DR+CD90+ synovial fibroblasts.

中文翻译:

JAK 抑制对干扰素-γ 诱导促炎性 HLA–DR+CD90+ 类风湿性关节炎滑膜成纤维细胞的影响

最近对类风湿性关节炎 (RA) 患者的滑膜进行转录组分析的结果表明,扩增 15 倍的 HLA–DR+CD90+ 滑膜成纤维细胞可能是炎症的关键介质。HLA–DR+CD90+ 滑膜成纤维细胞扩增的原因尚不清楚,但遗传特征表明干扰素-γ (IFNγ) 在该成纤维细胞亚群的产生中起着核心作用。本研究旨在调查 HLA–DR+CD90+ 滑膜成纤维细胞的产生、功能和治疗预期阻断。
更新日期:2021-08-25
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