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

Citation

Verified title: Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus
Publication year: 2011
DOI: 10.1038/ni.2131
Metadata source: crossref-doi (confidence: high)
Original local title: Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus

Ingest Mode

Mode: focused manual crystallization mode
Meaning: this source page has been manually upgraded for a priority crystallization pass and may support durable topic/entity/project/digest synthesis.
Required boundary: reusable claims from this source still need source-linked species, tissue, assay, model, and confidence labels.

Source Type

primary research article
mouse and human lung ILC characterization with influenza repair model
amphiregulin-linked tissue homeostasis source
crystallization status: manually promoted into batch 1 high-priority lung ILC source note

Evidence Profile

Overall confidence: high for lung ILC accumulation after influenza and amphiregulin-associated restoration of epithelial integrity in the mouse model.
Directness to this project: high for lung ILC repair/homeostasis after respiratory viral infection.
Evidence type: lung ILC phenotyping in mice and humans, ILC depletion, influenza infection, epithelial integrity and lung function readouts, amphiregulin rescue.
Main biological axis: influenza injury -> lung-resident/accumulating ILCs -> amphiregulin -> epithelial repair and lung function preservation.

Why It Matters Here

This is the paired repair-side source for viral lung ILC biology. It prevents the wiki from treating infection-induced ILC activation as purely pathogenic by showing that lung ILCs can restore epithelial integrity after influenza injury.

Key Findings

The study identified lung-resident ILCs in mice and humans expressing markers including Thy-1/CD90, CD25, CD127, and ST2.
Mouse lung ILCs accumulated after influenza infection.
Depletion of ILCs caused loss of airway epithelial integrity, reduced lung function, and impaired airway remodeling.
Administration of amphiregulin restored the defects caused by ILC depletion.

Claim-Level Confidence

High confidence: lung ILCs contribute to epithelial repair and lung function preservation after influenza infection in this mouse model.
High confidence: amphiregulin is a key ILC-associated repair mediator in this source.
Medium confidence: the human lung ILC identification supports relevance beyond mouse, but functional repair evidence is strongest in the mouse model.
Low confidence: this source alone does not establish that all ILC2 activation during viral infection is protective.

Methods and Context

Influenza A/Puerto Rico/8/34 H1N1 infection model.
Lung ILC phenotyping in mouse and human samples.
ILC depletion and amphiregulin rescue used to test repair function.
Readouts include epithelial integrity, lung function, and airway remodeling.

Caveats

Broad ILC depletion can affect more than one ILC subset or state.
The reparative phenotype is context- and time-dependent; it should be interpreted alongside pathogenic viral-AHR sources.
Human evidence in this source is stronger for presence/phenotype than for direct functional repair.

Contradiction and Supersession

Contradiction/tension: complements rather than negates influenza-induced AHR literature; infection can reveal both pathogenic and repair-associated ILC functions.
Supersession status: not superseded; best used as the foundational lung ILC repair/homeostasis source.