Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus.
Nat Immunol, 2011/11;12(11):1045-54.
Monticelli LA[1], Sonnenberg GF, Abt MC, Alenghat T, Ziegler CG, Doering TA, Angelosanto JM, Laidlaw BJ, Yang CY, Sathaliyawala T, Kubota M, Turner D, Diamond JM, Goldrath AW, Farber DL, Collman RG, Wherry EJ, Artis D
Affiliations
PMID: 21946417DOI: 10.1031/ni.2131
Impact factor: 31.25
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.
MeSH terms
Airway Remodeling; Amphiregulin; Animals; Antigens, CD; Cells, Cultured; EGF Family of Proteins; Glycoproteins; Homeostasis; Humans; Immunity, Innate; Influenza, Human; Intercellular Signaling Peptides and Proteins; Interleukin-33; Interleukins; Lung; Mice; Mice, Inbred C57BL; Orthomyxoviridae; Orthomyxoviridae Infections; Respiratory Mucosa; Wound Healing
More resources
Full text:
Europe PubMed Central; PubMed Central
EndNote: Download