摘要 : Type I interferons (IFN) causes inflammatory responses to pathogens, and can be elevated in autoimmune diseases such as systemic lupus erythematosus (SLE). We previously reported unexpected associations of increased numbers of B l... 展开 Type I interferons (IFN) causes inflammatory responses to pathogens, and can be elevated in autoimmune diseases such as systemic lupus erythematosus (SLE). We previously reported unexpected associations of increased numbers of B lymphocytes expressing the DNA-binding protein ARID3a with both IFN alpha (IFN alpha) expression and increased disease activity in SLE. Here, we determined that IFN alpha producing low density neutrophils (LDNs) and plasmacytoid dendritic cells (pDCs) from SLE patients exhibit strong associations between ARID3a protein expression and IFN alpha production. Moreover, SLE disease activity indices correlate most strongly with percentages of ARID3a(+) LDNs, but were also associated, less significantly, with IFN alpha expression in LDNs and pDCs. Hierarchical clustering and transcriptome analyses of LDNs and pDCs revealed SLE patients with low ARID3a expression cluster with healthy controls and identified gene profiles associated with increased proportions of ARID3a- and IFN alpha-expressing cells of each type. These data identify ARID3a as a potential transcription regulator of IFN alpha-related inflammatory responses and other pathways important for SLE disease activity. 收起