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Neurons reprogramme encephalitogenic T cells (T enc ) to regulatory T cells (T regs ), either FoxP3 + T regs  or FoxA1 + T regs . We reported previously that neuronal ability to generate FoxA1 + T regs  was central to preventing neuroinflammation in experimental autoimmune encephalomyelitis (EAE). Mice lacking interferon (IFN)-β were defective in generating FoxA1 + T regs  in the brain. Here we show that lack of neuronal IFNβ signalling is associated with the absence of programme death ligand-1 (PDL1), which prevents their ability to reprogramme T enc  cells to FoxA1 + T regs . Passive transfer-EAE via IFNβ-competent T enc  cells to mice lacking IFNβ and active induced-EAE in mice lacking its receptor, IFNAR, in the brain ( Nes   Cre   :Ifnar   fl/fl  ) result in defective FoxA1 + T regs  generation and aggravated neuroinflammation. IFNβ activates neuronal PI3K/Akt signalling and Akt binds to transcription factor FoxA1 that translocates to the nucleus and induces PDL1. Conversely, inhibition of PI3K/Akt, FoxA1 and PDL1 blocked neuronal ability to generate FoxA1 + T regs . We characterize molecular factors central for neuronal ability to reprogramme pathogenic T cells to FoxA1 + T regs  preventing neuroinflammation.

Neuronal IFN-beta–induced PI3K/Akt-FoxA1 signalling is essential for generation of FoxA1+Treg cells