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

Chizuko Miyamoto, Satoshi Kojo, Motoi Yamashita, Kazuyo Moro, Georges Lacaud, Katsuyuki Shiroguchi, Ichiro Taniuchi and Takashi Ebihara ()
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Chizuko Miyamoto: RIKEN Center for Integrative Medical Sciences (IMS)
Satoshi Kojo: RIKEN Center for Integrative Medical Sciences (IMS)
Motoi Yamashita: RIKEN Center for Integrative Medical Sciences (IMS)
Kazuyo Moro: RIKEN Center for Integrative Medical Sciences (IMS)
Georges Lacaud: The University of Manchester
Katsuyuki Shiroguchi: RIKEN Center for Integrative Medical Sciences (IMS)
Ichiro Taniuchi: RIKEN Center for Integrative Medical Sciences (IMS)
Takashi Ebihara: RIKEN Center for Integrative Medical Sciences (IMS)

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41467-019-08365-0

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