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T helper 17 (T17) cells are thought to play an important role in the pathogenesis of many autoimmune disorders, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, recent studies have suggested that interleukin-17 (IL-17) may be dispensable for the induction of EAE. Here, we use an adoptive transfer model of EAE to demonstrate that an adaptive cellular source of IL-17 is absolutely required for the induction of EAE disease. We further show that B cells can regulate the transfer of EAE disease in this context. Transcriptional profiling of T17 cells in our model suggests that loss of IL-17A/F in T cells results in a lack of an IL-23 receptor (IL-23R)-driven signaling signature. Our data demonstrate the critical importance of an adaptive immune cellular source of IL-17A and IL-17F to mediate EAE and that IL-17 signaling is required for IL-23-mediated T17 cell pathogenicity.