TRIM22 and systemic lupus erythematosus: IRF7 has been established as an SLE genetic risk locus that alters IFN type I expression21 and TRIM molecules have been studied as autoantigens in some autoimmune diseases, especially in Sjögren’s syndrome (SS) where TRIM22 protein showed little or no immunoreactivity in a sub-population of SS patients23 suggesting that TRIM22 was acting as a potential SSA60 regulated gene.