Our data therefore suggests a novel mechanism by which TRIM21 activity is regulated via promoting interaction with its substrate and provides insights into TRIM21 activity that may be manipulated in order to regulate type I IFN production in the treatment of autoimmune disorders such as SLE, in which overproduction of type I IFN and IL-23 play an important role in the pathogenesis of the disease. This evidence concerns the gene TRIM21 and systemic lupus erythematosus.