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

TitleInnate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus.
Publication TypeJournal Article
Year of Publication2011
AuthorsMonticelli LA, Sonnenberg GF, Abt MC, Alenghat T, Ziegler CGK, Doering TA, Angelosanto JM, Laidlaw BJ, Yang CY, Sathaliyawala T, Kubota M, Turner D, Diamond JM, Goldrath AW, Farber DL, Collman RG, E Wherry J, Artis D
JournalNat Immunol
Volume12
Issue11
Pagination1045-54
Date Published2011 Nov
ISSN1529-2916
KeywordsAirway Remodeling, Amphiregulin, Animals, Antigens, CD, Cells, Cultured, EGF Family of Proteins, Glycoproteins, Homeostasis, Humans, Immunity, Innate, Influenza, Human, Intercellular Signaling Peptides and Proteins, Interleukins, Lung, Mice, Mice, Inbred C57BL, Orthomyxoviridae, Orthomyxoviridae Infections, Respiratory Mucosa, Wound Healing
Abstract

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 a-chain (CD25), IL-7 receptor a-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.

DOI10.1031/ni.2131
Alternate JournalNat. Immunol.
PubMed ID21946417
PubMed Central IDPMC3320042
Grant ListAI061570 / AI / NIAID NIH HHS / United States
AI071309 / AI / NIAID NIH HHS / United States
AI074878 / AI / NIAID NIH HHS / United States
AI087990 / AI / NIAID NIH HHS / United States
AI091759 / AI / NIAID NIH HHS / United States
AI095466 / AI / NIAID NIH HHS / United States
AI095608 / AI / NIAID NIH HHS / United States
DK50306 / DK / NIDDK NIH HHS / United States
HHSN266200500030C / / PHS HHS / United States
HL098957 / HL / NHLBI NIH HHS / United States
K08 DK093784 / DK / NIDDK NIH HHS / United States
R01 AI067545 / AI / NIAID NIH HHS / United States
R01 AI072117 / AI / NIAID NIH HHS / United States
T32 AI007532 / AI / NIAID NIH HHS / United States
T32AI007532 / AI / NIAID NIH HHS / United States
T32AI05528 / AI / NIAID NIH HHS / United States
U01AI095608 / AI / NIAID NIH HHS / United States
U19 AI083022 / AI / NIAID NIH HHS / United States
U19 AI083022-01 / AI / NIAID NIH HHS / United States
U19 AI083022-02 / AI / NIAID NIH HHS / United States
U19 AI083022-03 / AI / NIAID NIH HHS / United States
U19 AI083022-04 / AI / NIAID NIH HHS / United States
U19AI083022 / AI / NIAID NIH HHS / United States

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