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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.

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