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00925njm 22002777a 4500 dc Tullius, Stefan G. author Rodriguez-Cetina Biefer, Héctor author Li, Suyan author Trachtenberg, Alexander J. author Edtinger, Karoline author Quante, Markus author Krenzien, Felix author Uehara, Hirofumi author Yang, Xiaoyong author Kissick, Haydn T. author Kuo, Winston P. author Ghiran, Ionita author Fuente García, Miguel Ángel de la author Arredouani, Mohamed S. author Camacho, Virginia author Tigges, John C. author Toxavidis, Vasilis author El Fatimy, Rachid author Smith, Brian D. author Vasudevan, Anju author Elkhal, Abdallah author 2014 CD4(+) T cells are involved in the development of autoimmunity, including multiple sclerosis (MS). Here we show that nicotinamide adenine dinucleotide (NAD(+)) blocks experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by inducing immune homeostasis through CD4(+)IFNγ(+)IL-10(+) T cells and reverses disease progression by restoring tissue integrity via remyelination and neuroregeneration. We show that NAD(+) regulates CD4(+) T-cell differentiation through tryptophan hydroxylase-1 (Tph1), independently of well-established transcription factors. In the presence of NAD(+), the frequency of T-bet(-/-) CD4(+)IFNγ(+) T cells was twofold higher than wild-type CD4(+) T cells cultured in conventional T helper 1 polarizing conditions. Our findings unravel a new pathway orchestrating CD4(+) T-cell differentiation and demonstrate that NAD(+) may serve as a powerful therapeutic agent for the treatment of autoimmune and other diseases. Nature Communications, 2014, 5, Article number: 5101 2041-1723 http://uvadoc.uva.es/handle/10324/9465 10.1038/ncomms6101 Nature Communications 5 Inmunología Medicamentos - Investigación NADþ protects against EAE by regulating CD4þ T-cell differentiation