Collectively, our results therefore indicates that IRF5 is a novel target for TRIM21 and that dysregulation of TRIM21 activity in SLE may thus contribute to enhanced IRF5 levels and consequently to the enhanced levels of type I IFN and pro-inflammatory cytokines, in part regulated by IRF5, observed in SLE patients [44], [45]. This evidence concerns the gene IRF5 and systemic lupus erythematosus.