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
The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2
University of Chicago, IL 60637 USA.
University of Chicago, IL 60637 USA.
University of Chicago, IL 60637 USA.
University of Chicago, IL 60637 USA.
Show others and affiliations
2016 (English)In: Journal of Experimental Medicine, ISSN 0022-1007, E-ISSN 1540-9538, Vol. 213, no 5, 687-696 p.Article in journal (Refereed) Published
Abstract [en]

Group 2 innate lymphoid cells ( ILC2s) are a subset of ILCs that play a protective role in the response to helminth infection, but they also contribute to allergic lung inflammation. Here, we report that the deletion of the ETS1 transcription factor in lymphoid cells resulted in a loss of ILC2s in the bone marrow and lymph nodes and that ETS1 promotes the fitness of the common progenitor of all ILCs. ETS1-deficient ILC2 progenitors failed to up-regulate messenger RNA for the E protein transcription factor inhibitor ID2, a critical factor for ILCs, and these cells were unable to expand in cytokine-driven in vitro cultures. In vivo, ETS1 was required for the IL-33-induced accumulation of lung ILC2s and for the production of the T helper type 2 cytokines IL-5 and IL-13. IL-25 also failed to elicit an expansion of inflammatory ILC2s when these cells lacked ETS1. Our data reveal ETS1 as a critical regulator of ILC2 expansion and cytokine production and implicate ETS1 in the regulation of Id2 at the inception of ILC2 development.

Place, publisher, year, edition, pages
ROCKEFELLER UNIV PRESS , 2016. Vol. 213, no 5, 687-696 p.
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-131199DOI: 10.1084/jem.20150851ISI: 000380845500006PubMedID: 27069114OAI: oai:DiVA.org:liu-131199DiVA: diva2:971889
Note

Funding Agencies|National Institutes of Health [R01 AI106352, R21 AI115388, R01 HL071063, T32AI007090, F32CA177235]; Rafael Rivera Asthma Research Fund; Leukemia and Lymphoma Society

Available from: 2016-09-19 Created: 2016-09-12 Last updated: 2017-11-21

Open Access in DiVA

fulltext(1688 kB)33 downloads
File information
File name FULLTEXT01.pdfFile size 1688 kBChecksum SHA-512
09ed9c96bd96e35019a9259b8f25003e8577617eebb9d451f89544bdb4a40d33ef1987d9ea5d9a03099dded5337a9feed895ae5af4f799268b2de9d34b48cdc7
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
In the same journal
Journal of Experimental Medicine
Cell and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar
Total: 33 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: 37 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