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Immunity
Article
License: Elsevier Non-Commercial
Data sources: UnpayWall
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Immunity
Article . 2012
License: Elsevier Non-Commercial
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Immunity
Article . 2012 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
Immunity
Article . 2012
Data sources: Pure Amsterdam UMC
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The Transcription Factor GATA3 Is Essential for the Function of Human Type 2 Innate Lymphoid Cells

Authors: Mjösberg, Jenny; Bernink, Jochem; Golebski, Korneliusz; Karrich, Julien J.; Peters, Charlotte P.; Blom, Bianca; te Velde, Anje A.; +3 Authors

The Transcription Factor GATA3 Is Essential for the Function of Human Type 2 Innate Lymphoid Cells

Abstract

Type 2 innate lymphoid cells (ILC2s) are part of a large family of ILCs that are important effectors in innate immunity, lymphoid organogenesis, and tissue remodeling. ILC2s mediate parasite expulsion but also contribute to airway inflammation, emphasizing the functional similarity between these cells and Th2 cells. Consistent with this, we report that the transcription factor GATA3 was highly expressed by human ILC2s. CRTH2(+) ILC2s were enriched in nasal polyps of patients with chronic rhinosinusitis, a typical type 2-mediated disease. Nasal polyp epithelial cells expressed TSLP, which enhanced STAT5 activation, GATA3 expression, and type 2 cytokine production in ILC2s. Ectopic expression of GATA3 in Lin(-)CD127(+)CRTH2(-) cells resulted in induction of CRTH2 and the capacity to produce high amounts of type 2 cytokines in response to TSLP plus IL-33. Hence, we identify GATA3, potently regulated by TSLP, as an essential transcription factor for the function of human ILC2s.

Country
Netherlands
Related Organizations
Keywords

Interleukin-13, Immunology, GATA3 Transcription Factor, Epithelium, Immunity, Innate, Cell Line, Infectious Diseases, Nasal Polyps, Gene Expression Regulation, Thymic Stromal Lymphopoietin, STAT5 Transcription Factor, Immunology and Allergy, Cytokines, Humans, Lymphocytes, Receptors, Cytokine

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    selected citations
    These citations are derived from selected sources.
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    585
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 0.1%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 1%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 0.1%
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
585
Top 0.1%
Top 1%
Top 0.1%
hybrid