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    Androgen signaling negatively controls group 2 innate lymphoid cells

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    Author
    Laffont, S; Blanquart, E; Savignac, M; Cenac, C; Laverny, G; Metzger, D; Girard, J-P; Belz, GT; Pelletier, L; Seillet, C; ...
    Date
    2017-06-01
    Source Title
    Journal of Experimental Medicine
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Belz, Gabrielle; Seillet, Cyril
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Laffont, S., Blanquart, E., Savignac, M., Cenac, C., Laverny, G., Metzger, D., Girard, J. -P., Belz, G. T., Pelletier, L., Seillet, C. & Guery, J. -C. (2017). Androgen signaling negatively controls group 2 innate lymphoid cells. JOURNAL OF EXPERIMENTAL MEDICINE, 214 (6), pp.1581-1592. https://doi.org/10.1084/jem.20161807.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259116
    DOI
    10.1084/jem.20161807
    Abstract
    Prevalence of asthma is higher in women than in men, but the mechanisms underlying this sex bias are unknown. Group 2 innate lymphoid cells (ILC2s) are key regulators of type 2 inflammatory responses. Here, we show that ILC2 development is greatly influenced by male sex hormones. Male mice have reduced numbers of ILC2 progenitors (ILC2Ps) and mature ILC2s in peripheral tissues compared with females. In consequence, males exhibit reduced susceptibility to allergic airway inflammation in response to environmental allergens and less severe IL-33-driven lung inflammation, correlating with an impaired expansion of lung ILC2s. Importantly, orchiectomy, but not ovariectomy, abolishes the sex differences in ILC2 development and restores IL-33-mediated lung inflammation. ILC2Ps express the androgen receptor (AR), and AR signaling inhibits their differentiation into mature ILC2s. Finally, we show that hematopoietic AR expression limits IL-33-driven lung inflammation through a cell-intrinsic inhibition of ILC2 expansion. Thus, androgens play a crucial protective role in type 2 airway inflammation by negatively regulating ILC2 homeostasis, thereby limiting their capacity to expand locally in response to IL-33.

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