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Gut reaction to IL-17
Whether IL-17A/F or TH17 cells are necessary for the immunopathogenesis of human multiple sclerosis (MS) has been a topic of active debate. Using experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, in mice deficient for IL-17A and IL-17F, Regen et al. found that IL-17 ablation reduced susceptibility to EAE. However, adoptive transfer of TH17 cells from autoantigen-primed IL-17–deficient mice recapitulated disease in naïve control mice but not in IL-17–deficient mice. Cohousing IL-17–deficient mice with IL-17–expressing mice, fecal transplantation from IL-17–expressing mice into IL-17–deficient mice, and reexpression of IL-17A in the gut of IL-17–deficient mice restored susceptibility to EAE. Thus, IL-17 expression in the gut rather than its effector function in the CNS is directly linked to EAE susceptibility by modulating the gut microbiome.
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