RT info:eu-repo/semantics/article
T1 NADþ protects against EAE by regulating CD4þ T-cell differentiation
A1 Tullius, Stefan G.
A1 Rodriguez-Cetina Biefer, Héctor
A1 Li, Suyan
A1 Trachtenberg, Alexander J.
A1 Edtinger, Karoline
A1 Quante, Markus
A1 Krenzien, Felix
A1 Uehara, Hirofumi
A1 Yang, Xiaoyong
A1 Kissick, Haydn T.
A1 Kuo, Winston P.
A1 Ghiran, Ionita
A1 Fuente García, Miguel Ángel de la
A1 Arredouani, Mohamed S.
A1 Camacho, Virginia
A1 Tigges, John C.
A1 Toxavidis, Vasilis
A1 El Fatimy, Rachid
A1 Smith, Brian D.
A1 Vasudevan, Anju
A1 Elkhal, Abdallah
K1 Inmunología
K1 Medicamentos - Investigación
AB 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.
PB Nature Publish Group
SN 2041-1723
YR 2014
FD 2014
LK http://uvadoc.uva.es/handle/10324/9465
UL http://uvadoc.uva.es/handle/10324/9465
LA eng
NO Nature Communications, 2014, 5, Article number: 5101
NO Producción Científica
DS UVaDOC
RD 23-abr-2024