We show here that IFNAR expression by B cells contributes to increased levels of anti-chromatin IgG, anti-dsDNA and anti-nRNP IgG and IgG2c autoantibodies in lupus-prone B6.Nba2 mice, without significantly increasing total levels of IgG or IgM and without skewing total IgG subtype presentation. This evidence concerns the gene IFNAR1 and systemic lupus erythematosus.