Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity

Ya Jen Chang, Hye Young Kim, Lee A. Albacker, Nicole Baumgarth, Andrew N J McKenzie, Dirk E. Smith, Rosemarie H. Dekruyff, Dale T. Umetsu

Research output: Contribution to journalArticle

547 Scopus citations

Abstract

Patients with asthma, a major public health problem, are at high risk for serious disease from influenza virus infection, but the pathogenic mechanisms by which influenza A causes airway disease and asthma are not fully known. We show here in a mouse model that influenza infection acutely induced airway hyper-reactivity (AHR), a cardinal feature of asthma, independently of T helper type 2 (TH2) cells and adaptive immunity. Instead, influenza infection induced AHR through a previously unknown pathway that required the interleukin 13 (IL-13)-IL-33 axis and cells of the non-T cell, non-B cell innate lymphoid type called 'natural helper cells'. Infection with influenza A virus, which activates the NLRP3 inflammasome, resulted in much more production of IL-33 by alveolar macrophages, which in turn activated natural helper cells producing substantial IL-13.

Original languageEnglish (US)
Pages (from-to)631-638
Number of pages8
JournalNature Immunology
Volume12
Issue number7
DOIs
StatePublished - May 2011

ASJC Scopus subject areas

  • Immunology

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    Chang, Y. J., Kim, H. Y., Albacker, L. A., Baumgarth, N., McKenzie, A. N. J., Smith, D. E., Dekruyff, R. H., & Umetsu, D. T. (2011). Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity. Nature Immunology, 12(7), 631-638. https://doi.org/10.1038/ni.2045