PGE2, the derivative of AA, is proven to exert dual roles in mouse experimental autoimmune encephalomyelitis, facilitating Th1 and Th17 cell generation redundantly through PGE receptor 4 (EP4) and EP2, meanwhile, weakening the invasion of these T cells into the brain by guarding blood-brain barrier through EP4 (52). This evidence concerns the gene PTGER4 and experimental autoimmune encephalomyelitis.