Innate lymphoid cells in lung infection and immunity
Citation
- Verified title: Innate lymphoid cells in lung infection and immunity
- Publication year: 2018
- DOI: 10.1111/imr.12712
- Metadata source: crossref-doi (confidence: high)
- Original local title: Innate lymphoid cells in lung infection and immunity
Ingest Mode
- Mode:
focused manual crystallization mode - Meaning: this source page was manually reviewed for source text, model context, assay directness, and claim boundaries.
- Durable synthesis status: selected source-specific claims were propagated into entity/topic/digest pages only where evidence strength and context labels are preserved.
Source Type
- review of ILCs in lung infection and immunity
- Evidence profile: lung-invading pathogen map, ILC subset effector functions, and review-level synthesis across viral, bacterial, fungal, and helminth contexts.
- Knowledge note status: source-reviewed review note suitable for lung infection routing and evidence-map context.
Evidence Profile
- Overall confidence: medium for review-level pathogen-to-ILC mapping; lower for mechanistic strength unless traced to primary sources.
- Evidence tags: #source/review #species/mixed #tissue/lung #cell/ILC1 #cell/ILC2 #cell/ILC3 #cell/NK #outcome/infection #outcome/repair #outcome/inflammation #axis/ILC_lung_infection #status/focused_crystallization
- Primary biological axis: lung pathogens engage different ILC modules, including ILC2 repair/type 2 programs and ILC3 IL-17/IL-22 bacterial-defense programs.
Why It Matters Here
This review is a useful reference-map page for readers entering the lung infection branch. It links pathogen classes to ILC outputs but should remain a route into primary source notes rather than a high-confidence mechanistic anchor.
Key Findings
- The review organizes lung ILC responses across respiratory viruses, bacterial pathogens such as Streptococcus pneumoniae and Mycobacterium tuberculosis, fungal infection, and helminth contexts.
- It highlights ILC2-derived amphiregulin/IL-5/IL-13 and ILC3-derived IL-17/IL-22 as recurring lung infection or repair mediators.
- It underscores that lung ILCs can contribute to both protection and immune pathology depending on pathogen and timing.
- The page is best used as a disease-orientation map for source navigation.
Claim-Level Confidence
- Medium confidence: lung infection is a major organizing context for ILC2 and ILC3 biology.
- Low-to-medium confidence: specific mediator-pathogen claims should be checked against cited primary papers.
- Low confidence: this review should not be used alone to make causal or therapeutic claims.
Methods and Context
- Source type: narrative review.
- Evidence directness: synthesis across primary studies.
- Best wiki use: infection reading route, pathogen table interpretation, and lung ILC subset overview.
Caveats
- Pathogen categories should not be collapsed; influenza, RSV, pneumococcus, Mtb, and fungi differ sharply.
- Review tables may include unpublished or preliminary context; cite primary sources for durable claims.
- Protective and pathogenic ILC roles must be time- and model-labeled.
Contradiction and Supersession
- Contradiction status: explains why infection sources may show both repair and pathology.
- Supersession status: not superseded; use as an orientation layer.
Related Pages
- ILC2
- ILC3
- ILC2 roles in pulmonary disease
- ILC2 functional regulation mechanisms
- ILC3 roles in pulmonary disease
- ILC3 functional regulation mechanisms
- Lung ILC Core Evidence Synthesis
- ILC In Lung