Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus

Laurel A. Monticelli, Gregory F. Sonnenberg, Michael C. Abt, Theresa Alenghat, Carly G.K. Ziegler, Travis A. Doering, Jill M. Angelosanto, Brian J. Laidlaw, Cliff Y. Yang, Taheri Sathaliyawala, Masaru Kubota, Damian Turner, Joshua M. Diamond, Ananda W. Goldrath, Donna L. Farber, Ronald G. Collman, E. John Wherry, David Artis

Research output: Contribution to journalArticlepeer-review

1212 Scopus citations


Innate lymphoid cells (ILCs), a heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor α-chain (CD25), IL-7 receptor α-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus.

Original languageEnglish
Pages (from-to)1045-1054
Number of pages10
JournalNature immunology
Issue number11
StatePublished - Nov 2011


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