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    Runx/Cbfbeta complexes protect group 2 innate lymphoid cells from exhausted-like hyporesponsiveness during allergic airway inflammation.

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    Authors
    Miyamoto, C
    Kojo, S
    Yamashita, M
    Moro, K
    Lacaud, Georges
    Shiroguchi, K
    Taniuchi, I
    Ebihara, T
    Affiliation
    Laboratory for Transcriptional Regulation, RIKEN Center for Integrative Medical Sciences (IMS), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, 230-0045, Japan
    Issue Date
    2019
    
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    Abstract
    Group 2 innate lymphoid cells (ILC2s) have tissue-resident competence and contribute to the pathogenesis of allergic diseases. However, the mechanisms regulating prolonged ILC2-mediated TH2 cytokine production under chronic inflammatory conditions are unclear. Here we show that, at homeostasis, Runx deficiency induces excessive ILC2 activation due to overly active GATA-3 functions. By contrast, during allergic inflammation, the absence of Runx impairs the ability of ILC2s to proliferate and produce effector TH2 cytokines and chemokines. Instead, functional deletion of Runx induces the expression of exhaustion markers, such as IL-10 and TIGIT, on ILC2s. Finally, these 'exhausted-like' ILC2s are unable to induce type 2 immune responses to repeated allergen exposures. Thus, Runx confers competence for sustained ILC2 activity at the mucosa, and contributes to allergic pathogenesis
    Citation
    Miyamoto C, Kojo S, Yamashita M, Moro K, Lacaud G, Shiroguchi K, et al. Runx/Cbfbeta complexes protect group 2 innate lymphoid cells from exhausted-like hyporesponsiveness during allergic airway inflammation. Nat Commun. 2019 Jan 25;10(1):447.
    Journal
    Nature Communications
    URI
    http://hdl.handle.net/10541/621600
    DOI
    10.1038/s41467-019-08365-0
    PubMed ID
    30683858
    Additional Links
    https://dx.doi.org/10.1038/s41467-019-08365-0
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41467-019-08365-0
    Scopus Count
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    All Paterson Institute for Cancer Research

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