In the context of human autoimmune disease, IL-17-producing FOXP3+ Tregs with in vitro suppressive capacity have been shown to be recruited to the intestinal mucosa in active Crohn's disease patients [75], to the inflamed joints of juvenile idiopathic arthritis (JIA) patients [68] and to peripheral blood of rheumatoid arthritis patients [76]. Here, FOXP3 is linked to rheumatoid arthritis.