A recent report [20] shows that CCR6+ memory T-helper cells producing IL-17A, IL-17F, IL-21, and/or IL-22 are increased in SLE patients and that this increase is related to the presence of IFN type I signature thus providing evidence that IFN type I signature co-acts with Th17 cells and related cytokines in the pathogenesis of systemic autoimmune diseases such as SLE. Here, IL17A is linked to systemic lupus erythematosus.