IL-17 controls CNS autoimmunity through the intestinal microbiome

IL-17A and IL-17F-producing CD4+ T cells (TH17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Further, TH17 cells orchestrate leukocyte invasion of the central nervous system (CNS) and subsequent tissue damage. However, the role of IL-17 as an effector cytokine is still confused with the encephalitogenic function of Th17 cells, fueling a longstanding debate in the Neuroimmunology field. Here, we demonstrate that mice deficient for IL-17A/F lose their susceptibility to EAE, due to an altered composition of their gut microbiota.