Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Id3 Maintains Foxp3 Expression in Regulatory T Cells by Controlling a TranscriptionalNetwork of E47, Spi-B, and SOCS3
University of Medical Centre Freiburg, Germany; University of Freiburg, Germany.
University of Medical Centre Freiburg, Germany; University of Freiburg, Germany.
University of Medical Centre Freiburg, Germany; University of Freiburg, Germany; Max Planck Institute Immunobiol and Epigenet, Germany.
University of Freiburg, Germany.
Show others and affiliations
2016 (English)In: CELL REPORTS, ISSN 2211-1247, Vol. 17, no 11, p. 2827-2836Article in journal (Refereed) Published
Abstract [en]

The transcription factor Foxp3 dominantly controls regulatory T (Treg) cell function, and only its continuous expression guarantees the maintenance of full Treg cell-suppressive capacity. However, transcriptional regulators maintaining Foxp3 transcription are incompletely described. Here, we report that high E47 transcription factor activity in Treg cells resulted in unstable Foxp3 expression. Under homeostatic conditions, Treg cells expressed high levels of the E47 antagonist Id3, thus restricting E47 activity and maintaining Foxp3 expression. In contrast, stimulation of Id3-deficient or E47-overexpressing Treg cells resulted in the loss of Foxp3 expression in a subset of Treg cells in vivo and in vitro. Mechanistic analysis indicated that E47 activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 expression. These findings demonstrate that the balance of Id3 and E47 controls the maintenance of Foxp3 expression in Treg cells and, thus, contributes to Treg cell plasticity.

Place, publisher, year, edition, pages
CELL PRESS , 2016. Vol. 17, no 11, p. 2827-2836
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-134213DOI: 10.1016/j.celrep.2016.11.045ISI: 000390894700004PubMedID: 27974197OAI: oai:DiVA.org:liu-134213DiVA, id: diva2:1069824
Note

Funding Agencies|International Graduate Academy fellowship; Max Planck Institute; German Research Foundation [DFG SCHA 1442/3-2, SCHA 1442/5-1]; Federal Ministry of Education and Research [BMBF 01EO1303]; European Commission [FP7 PIRG08-GA-2010-276906]; Muller-Fahnenberg Stiftung

Available from: 2017-01-30 Created: 2017-01-29 Last updated: 2018-01-13

Open Access in DiVA

fulltext(1781 kB)21 downloads
File information
File name FULLTEXT01.pdfFile size 1781 kBChecksum SHA-512
a5dd6a7498c7e5ee9378b80fd5f440ac95716dad95ed48f81375778605542be450aa3dc3a2b5ec8afa5a41bb38f6d22413a5f4ca0b337933fa5173124be1ef77
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Sigvardsson, Mikael
By organisation
Division of Microbiology and Molecular MedicineFaculty of Medicine and Health Sciences
Cell and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar
Total: 21 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 49 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf