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dc.contributor.authorElkhal, Abdallah
dc.contributor.authorRodriguez-Cetina Biefer, Héctor
dc.contributor.authorHeinbokel, Timm
dc.contributor.authorUehara, Hirofumi
dc.contributor.authorQuante, Markus
dc.contributor.authorSeyda, Midas
dc.contributor.authorSchuitenmaker, Jeroen M.
dc.contributor.authorKrenzien, Felix
dc.contributor.authorCamacho, Virginia
dc.contributor.authorFuente García, Miguel Ángel de la 
dc.contributor.authorGhiran, Ionita
dc.contributor.authorTullius, Stefan G.
dc.date.accessioned2021-01-07T11:30:18Z
dc.date.available2021-01-07T11:30:18Z
dc.date.issued2016
dc.identifier.citationScientific Reports, 2016, vol. 6. 12 p.es
dc.identifier.issn2045-2322es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/44633
dc.descriptionProducción Científicaes
dc.description.abstractCD4+ CD25+ Foxp3+ Tregs have been shown to play a central role in immune homeostasis while preventing from fatal inflammatory responses, while Th17 cells have traditionally been recognized as pro-inflammatory mediators implicated in a myriad of diseases. Studies have shown the potential of Tregs to convert into Th17 cells, and Th17 cells into Tregs. Increasing evidence have pointed out CD25 as a key molecule during this transdifferentiation process, however molecules that allow such development remain unknown. Here, we investigated the impact of NAD+ on the fate of CD4+ CD25+ Foxp3+ Tregs in-depth, dissected their transcriptional signature profile and explored mechanisms underlying their conversion into IL-17A producing cells. Our results demonstrate that NAD+ promotes Treg conversion into Th17 cells in vitro and in vivo via CD25 cell surface marker. Despite the reduced number of Tregs, known to promote homeostasis, and an increased number of pro-inflammatory Th17 cells, NAD+ was able to promote an impressive allograft survival through a robust systemic IL-10 production that was CD4+ CD25+ Foxp3+ independent. Collectively, our study unravels a novel immunoregulatory mechanism of NAD+ that regulates Tregs fate while promoting allograft survival that may have clinical applications in alloimmunity and in a wide spectrum of inflammatory conditions.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherSpringer Naturees
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.classificationT cellses
dc.subject.classificationCélulas Tes
dc.subject.classificationNicotinamide adenine dinucleotidees
dc.subject.classificationNicotinamida adenina dinucleótidoes
dc.titleNAD+ regulates Treg cell fate and promotes allograft survival via a systemic IL-10 production that is CD4+ CD25+ Foxp3+ T cells independentes
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2016 Springer Naturees
dc.identifier.doi10.1038/srep22325es
dc.relation.publisherversionhttps://www.nature.com/articles/srep22325es
dc.peerreviewedSIes
dc.description.projectNational Institutes of Health (grants R01AG039449 and R01HL096795)es
dc.description.projectGerman Research Foundation (grant KFO243/1)es
dc.description.projectInstituto de Salud Carlos III (grant PI10/02 511)es
dc.description.projectFundación Ramón Areces (grant CIVP16A1843)es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones


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