Adoptive transfer of RARα agonist-treated Tregs leads to improved Treg trafficking to gut tissue in a humanised mouse model of colitis.94 Supporting this mechanism for resolving inflammation, another group have demonstrated that DCs can be engineered de novo to produce high concentrations of RA.141 When transferred to mice, the RA-secreting DCs were able to augment the expression of Foxp3 and the gut-homing receptor CCR9 in native Tregs with the subsequent suppression of colitis. Here, FOXP3 is linked to colitis.