Interferon-α regulates abnormally increased expression of RSAD2 in Th17 and Tfh cells in systemic lupus erythematosus patients

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-alpha, 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-alpha.

Automated summary

In this study, higher expression levels of RSAD2 were observed in CD4(+) T-cell subsets from the peripheral blood of SLE patients, suggesting its regulatory role in the pathogenesis of SLE. The expression of RSAD2 in CD4(+) T cells may be regulated by IFN-alpha and significantly affects the differentiation of Th17 and Tfh cells.