Knockout of PD-L2 results in the excessed IFNγ production in Th1 cells.34 CCR6 is induced by TGFβ stimulation, which is important for the differentiation of Th17 and iTreg cells.35 Lack of CCR6 in Th17 cells reduces the severity of experimental autoimmune encephalomyelitis and Th17 and Treg recruitment into inflammatory tissues. Here, PDCD1LG2 is linked to experimental autoimmune encephalomyelitis.