An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis I

However, recent studies suggest that interleukin (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 TH17 cells in our model suggest that loss of IL-17A/F in T cells results in a lack of an IL-23 receptor (IL23R)–driven signaling signature. Our data demonstrates 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 TH17 cell pathogenicity.