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dc.contributor.authorSidwell, Tom
dc.contributor.authorLiao, Yang
dc.contributor.authorGarnham, Alexandra L
dc.contributor.authorVasanthakumar, Ajithkumar
dc.contributor.authorGloury, Renee
dc.contributor.authorBlume, Jonas
dc.contributor.authorTeh, Peggy P
dc.contributor.authorChisanga, David
dc.contributor.authorThelemann, Christoph
dc.contributor.authorRivera, Fabian de Labastida
dc.contributor.authorEngwerda, Christian R
dc.contributor.authorCorcoran, Lynn
dc.contributor.authorKometani, Kohei
dc.contributor.authorKurosaki, Tomohiro
dc.contributor.authoret al.
dc.date.accessioned2020-06-26T03:03:04Z
dc.date.available2020-06-26T03:03:04Z
dc.date.issued2020
dc.identifier.issn2041-1723
dc.identifier.doi10.1038/s41467-019-14112-2
dc.identifier.urihttp://hdl.handle.net/10072/394946
dc.description.abstractDifferentiation and homeostasis of Foxp3+ regulatory T (Treg) cells are strictly controlled by T-cell receptor (TCR) signals; however, molecular mechanisms that govern these processes are incompletely understood. Here we show that Bach2 is an important regulator of Treg cell differentiation and homeostasis downstream of TCR signaling. Bach2 prevents premature differentiation of fully suppressive effector Treg (eTreg) cells, limits IL-10 production and is required for the development of peripherally induced Treg (pTreg) cells in the gastrointestinal tract. Bach2 attenuates TCR signaling-induced IRF4-dependent Treg cell differentiation. Deletion of IRF4 promotes inducible Treg cell differentiation and rescues pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalizes eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracts the DNA-binding activity of IRF4 and limits chromatin accessibility, thereby attenuating IRF4-dependent transcription. Thus, Bach2 balances TCR signaling induced transcriptional activity of IRF4 to maintain homeostasis of thymically-derived and peripherally-derived Treg cells.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofpagefrom252:1
dc.relation.ispartofpageto252:17
dc.relation.ispartofissue1
dc.relation.ispartofjournalNature Communications
dc.relation.ispartofvolume11
dc.subject.fieldofresearchBiological sciences
dc.subject.fieldofresearchcode31
dc.subject.keywordsScience & Technology
dc.subject.keywordsMultidisciplinary Sciences
dc.subject.keywordsScience & Technology - Other Topics
dc.subject.keywordsFACTOR IRF4
dc.subject.keywordsDNA-METHYLATION
dc.titleAttenuation of TCR-induced transcription by Bach2 controls regulatory T cell differentiation and homeostasis
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationSidwell, T; Liao, Y; Garnham, AL; Vasanthakumar, A; Gloury, R; Blume, J; Teh, PP; Chisanga, D; Thelemann, C; Rivera, FDL; Engwerda, CR; Corcoran, L; Kometani, K; Kurosaki, T; et al., Attenuation of TCR-induced transcription by Bach2 controls regulatory T cell differentiation and homeostasis, NATURE COMMUNICATIONS, 2020, 11 (1), pp. 252:1-252:17
dcterms.dateAccepted2019-12-11
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/
dc.date.updated2020-06-26T02:58:48Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
gro.hasfulltextFull Text
gro.griffith.authorEngwerda, Christian R.


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