It has recently been demonstrated in experimental autoimmune encephalomyelitis (EAE) that IL-17A recruits IL-1β-secreting myeloid cells that prime pathogenic γδT17 and Th17 cells [108], whereas mice with HIF-1α-deficient T cells are resistant to induction of Th17-dependent EAE [23]. This evidence concerns the gene HIF1A and experimental autoimmune encephalomyelitis.