FOXP3 and colitis: When the Treg receptor TGF-βRI is lineage-specifically deleted in Foxp3+ cells, Foxp3+ Treg cells are unable to persist in the colon and thus fail to control colitis, suggesting that TGF-β has a tissue-specific effect on the regulation of Th17 cells by maintaining this Treg population at one of the sites of greatest Th17 cell accumulation23.