In several studies manipulation of ACKR2 levels modified tissue inflammation in a manner that would be predicted based on anti-inflammatory potency of ACKR2 as a chemokine scavenger: this was shown in experimental models of colitis and psoriasis, where deletion of ACKR2 increased colon [21] or skin [17] inflammation, and in inflamed NOD mouse islets where transgenic overexpression of ACKR2 reduced local islet inflammation [35]. This evidence concerns the gene ACKR2 and psoriasis.