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Feeding-dependent VIP neuron-ILC3 circuit regulates the intestinal barrier

Citation

  • Verified title: Feeding-dependent VIP neuron-ILC3 circuit regulates the intestinal barrier
  • Publication year: 2020
  • DOI: 10.1038/s41586-020-2039-9
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Feeding-dependent VIP neuron-ILC3 circuit regulates the intestinal barrier

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 neuroimmune ILC3 study
  • Evidence profile: feeding activates VIPergic neurons near VIPR2-positive ILC3s; VIPR2 engagement restrains ILC3 IL-22 and tunes barrier/metabolic responses.
  • 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 #tissue/gut #cell/ILC3 #assay/in_vivo #outcome/homeostasis #outcome/infection #axis/ILC_regulation #axis/neuroimmune #status/focused_crystallization
  • Primary biological axis: feeding activates VIPergic neurons near VIPR2-positive ILC3s; VIPR2 engagement restrains ILC3 IL-22 and tunes barrier/metabolic responses.

Why It Matters Here

This source adds feeding-dependent VIP neuron-ILC3 barrier circuit 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

  • Food intake activated VIP-producing enteric neurons near intestinal ILC3 clusters.
  • ILC3s expressed VIPR2/VPAC2.
  • VIPR2 engagement inhibited ILC3 IL-22 production in the reported context.
  • The source supports a feeding-dependent gut neuroimmune brake on ILC3 barrier output.

Claim-Level Confidence

  • High confidence: feeding-linked VIP neuron signals regulate gut ILC3 IL-22/barrier biology in the reported mouse model.
  • Medium confidence: VIP can act as an ILC3 neuroimmune regulatory axis.
  • Low confidence: lung ILC3 VIP regulation is not shown.

Methods and Context

  • Source-specific context: mouse feeding, enteric neuron, VIP/VIPR2, intestinal barrier and ILC3 functional assays.
  • 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

  • Separate VIPR2-mediated restraint from other VIP/VPAC1 recruitment findings.
  • 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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