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Trained ILC3 responses promote intestinal defense

Citation

  • Verified title: Trained ILC3 responses promote intestinal defense
  • Publication year: 2022
  • DOI: 10.1126/science.aaz8777
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Trained ILC3 responses promote intestinal defense

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page has been manually reviewed for the ILC3 mucosal-regulation question, including model system, tissue compartment, regulatory mediator, assay directness, and claim-level boundaries.
  • Required boundary: reusable claims should preserve species, tissue, mediator, disease model, and whether evidence is primary perturbation or review-level synthesis.

Source Type

  • primary gut ILC3 trained-response study
  • Evidence profile: time-limited enterobacterial challenge leaves intestinal ILC3s in a durable activated state that improves later intestinal defense.
  • Knowledge note status: source-reviewed evidence note suitable for gut/mucosal ILC3 regulation context.

Evidence Profile

  • Overall confidence: medium-high to high for source-specific gut/mucosal ILC3 biology; low for direct lung extrapolation unless matched pulmonary data are present.
  • Evidence tags: #source/primary #species/mouse #species/human #tissue/gut #cell/ILC3 #assay/RNAseq #assay/flow #assay/in_vivo #outcome/infection #outcome/inflammation #axis/ILC_regulation #axis/trained_immunity #status/focused_crystallization
  • Primary biological axis: time-limited enterobacterial challenge leaves intestinal ILC3s in a durable activated state that improves later intestinal defense.

Why It Matters Here

This source adds trained ILC3 responses promote intestinal defense to the ILC3 regulatory map. It is useful for mechanism vocabulary and tissue-boundary-aware interpretation, but should not be promoted to direct lung causality without pulmonary evidence.

Key Findings

  • Intestinal ILC3s persisted for months in an activated state after time-restricted Citrobacter rodentium exposure.
  • The trained state supported enhanced protection against subsequent intestinal challenge in the reported model.
  • The source supports trained or memory-like innate defense logic for ILC3s.
  • It remains gut infection evidence, not direct lung ILC3 memory evidence.

Claim-Level Confidence

  • High confidence: prior enteric challenge can generate durable trained ILC3 responses in the reported mouse gut model.
  • Medium-high confidence: trained-immunity logic belongs in ILC3 regulatory architecture.
  • Low confidence: pulmonary ILC3 training is not shown.

Methods and Context

  • Source-specific context: mouse enteric challenge, longitudinal ILC3 state analysis, flow, RNA-seq, and reinfection/defense readouts.
  • Best wiki use: ILC3 functional regulation, mucosal barrier biology, and evidence-boundary framing.
  • Assay directness: strongest for the source tissue/model; indirect for lung disease unless lung data are present.

Caveats

  • Do not equate trained ILC3 responses with antigen-specific adaptive memory.
  • Preserve species, tissue compartment, mediator, and disease-model labels.
  • Reviews should frame the field; primary sources should anchor causal claims.

Contradiction and Supersession

  • Contradiction status: complements the current ILC3 regulatory map by adding gut/mucosal context rather than replacing lung-specific evidence.
  • Supersession status: not superseded; use alongside direct pulmonary ILC3 sources with explicit tissue labels.

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