Abstract：
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that often involves abnormal activation of regulatory IFN genes and regulation of B cells by CD4+ T cells. Radical S-adenosyl methionine domain containing 2 (RSAD2) is a viral suppressor protein regulated by type I IFN, and it has been proven to play an important regulatory role in SLE. However, the mechanism by which RSAD2 participates in the pathogenesis of SLE is unclear. In this study, we observed higher expression levels of RSAD2 in CD4+ T-cell subsets from the peripheral blood of SLE patients than in those from healthy controls by bioinformatics analysis and validation experiments. We analyzed the expression of RSAD2 in CD4+ T cells of patients with SLE and other autoimmune diseases. In addition, we found that the expression of RSAD2 in CD4+ T cells might be regulated by IFN-α, and RSAD2 significantly affected the differentiation of Th17 cells and T follicular helper (Tfh) cells. Our findings underlined that RSAD2 may promote B-cell activation by promoting the differentiation of Th17 and Tfh cells in SLE patients, a process that is regulated by IFN-α.
摘要：
系统性红斑狼疮（SLE）是一种慢性自身免疫性疾病，通常涉及调节性干扰素基因的异常激活和CD4T细胞对B细胞的调节。RSAD2是由I型干扰素（IFN）调节的病毒抑制蛋白，它已被证明在SLE中起着重要的调节作用。然而,RSAD2参与SLE发病机制尚不清楚。在这项研究中,通过生物信息学分析和验证实验,我们观察到SLE患者外周血CD4+T细胞亚群中RSAD2的表达水平高于HCs.我们分析了SLE和其他自身免疫性疾病患者的CD4T细胞中RSAD2的表达。此外,我们发现CD4+T细胞中RSAD2的表达可能受IFN-α的调控,RSAD2明显影响Th17细胞和Tfh细胞的分化。我们的发现强调RSAD2可能通过促进SLE患者Th17和Tfh细胞的分化来促进B细胞活化。由IFN-α调节的过程。本文受版权保护。保留所有权利。
