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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.
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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
URN: urn:nbn:se:liu:diva-131199DOI: 10.1084/jem.20150851ISI: 000380845500006PubMedID: 27069114OAI: diva2:971889

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: 2016-10-12

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Sigvardsson, Mikael
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