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dc.contributor.authorKarwacz, Katarzyna
dc.contributor.authorMiraldi, Emily R
dc.contributor.authorPokrovskii, Maria
dc.contributor.authorMadi, Asaf
dc.contributor.authorYosef, Nir
dc.contributor.authorWortman, Ivo
dc.contributor.authorChen, Xi
dc.contributor.authorWatters, Aaron
dc.contributor.authorCarriero, Nicholas
dc.contributor.authorAwasthi, Amit
dc.contributor.authorBonneau, Richard
dc.contributor.authorLittman, Dan
dc.contributor.authorKuchroo, Vijay K
dc.contributor.authorRegev, Aviv
dc.date.accessioned2018-07-02T20:19:15Z
dc.date.available2018-07-02T20:19:15Z
dc.date.issued2017-02
dc.date.submitted2016-08
dc.identifier.issn1529-2908
dc.identifier.issn1529-2916
dc.identifier.urihttp://hdl.handle.net/1721.1/116739
dc.description.abstractType 1 regulatory T cells (Tr1 cells) are induced by interleukin-27 (IL-27) and have critical roles in the control of autoimmunity and resolution of inflammation. We found that the transcription factors IRF1 and BATF were induced early on after treatment with IL-27 and were required for the differentiation and function of Tr1 cells in vitro and in vivo. Epigenetic and transcriptional analyses revealed that both transcription factors influenced chromatin accessibility and expression of the genes required for Tr1 cell function. IRF1 and BATF deficiencies uniquely altered the chromatin landscape, suggesting that these factors serve a pioneering function during Tr1 cell differentiation.en_US
dc.description.sponsorshipNational Cancer Institute (U.S.) (Grant P30-CA14051)en_US
dc.publisherNature Publishing Groupen_US
dc.relation.isversionofhttp://dx.doi.org/10.1038/NI.3683en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alikeen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/en_US
dc.sourcePMCen_US
dc.titleCritical role of IRF1 and BATF in forming chromatin landscape during type 1 regulatory cell differentiationen_US
dc.typeArticleen_US
dc.identifier.citationKarwacz, Katarzyna et al. “Critical Role of IRF1 and BATF in Forming Chromatin Landscape During Type 1 Regulatory Cell Differentiation.” Nature Immunology 18, 4 (February 2017): 412–421 © 2017 Nature America Inc, part of Springer Natureen_US
dc.contributor.departmentBroad Institute of MIT and Harvarden_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.mitauthorRegev, Aviv
dc.relation.journalNature Immunologyen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2018-07-02T19:35:27Z
dspace.orderedauthorsKarwacz, Katarzyna; Miraldi, Emily R; Pokrovskii, Maria; Madi, Asaf; Yosef, Nir; Wortman, Ivo; Chen, Xi; Watters, Aaron; Carriero, Nicholas; Awasthi, Amit; Regev, Aviv; Bonneau, Richard; Littman, Dan; Kuchroo, Vijay Ken_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0001-8567-2049
mit.licenseOPEN_ACCESS_POLICYen_US


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