LAUSR

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that often involves abnormal activation of regulatory interferon genes and regulation of B cells by CD4+ T cells. RSAD2 is a viral suppressor protein regulated by type I interferon (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 HCs 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 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. This article is protected by copyright. All rights reserved.