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Vasoactive intestinal peptide promotes host defense against enteric pathogens by modulating the recruitment of group 3 innate lymphoid cells

Citation

  • Verified title: Vasoactive intestinal peptide promotes host defense against enteric pathogens by modulating the recruitment of group 3 innate lymphoid cells
  • Publication year: 2021
  • DOI: 10.1073/pnas.2106634118
  • Metadata source: crossref-title (confidence: high)
  • Original local title: Vasoactive intestinal peptide promotes host defense against enteric pathogens by modulating the recruitment of group 3 innate lymphoid cells

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 VIP-ILC3 recruitment study
  • Evidence profile: VIP/VPAC1 promotes intestinal ILC3 recruitment, lymphoid tissue formation, RA-producing DC maintenance, CCR9 expression, IL-22, and enteric 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 #tissue/gut #cell/ILC3 #cell/dendritic_cell #assay/KO #assay/flow #assay/in_vivo #outcome/infection #outcome/homeostasis #axis/ILC_regulation #axis/neuroimmune #status/focused_crystallization
  • Primary biological axis: VIP/VPAC1 promotes intestinal ILC3 recruitment, lymphoid tissue formation, RA-producing DC maintenance, CCR9 expression, IL-22, and enteric defense.

Why It Matters Here

This source adds VIP promotes ILC3 recruitment for enteric 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

  • VIP promoted ILC3 recruitment to intestine through VPAC1, independent of microbiota or adaptive immunity in the reported model.
  • VIP supported postnatal lymphoid tissue formation and local RA-producing dendritic-cell maintenance.
  • RA upregulated gut-homing receptor CCR9 on ILC3s.
  • VIP/VPAC1 deficiency reduced intestinal ILC3s, IL-22 output, and resistance to Citrobacter rodentium.

Claim-Level Confidence

  • High confidence: VIP/VPAC1 promotes gut ILC3 recruitment and enteric defense in the reported mouse system.
  • Medium confidence: VIP effects on ILC3 can be receptor- and context-dependent.
  • Low confidence: pulmonary ILC3 recruitment by VIP is not shown here.

Methods and Context

  • Source-specific context: mouse VIP/VPAC1 perturbation, gut ILC3 recruitment, RA/DC context, and enteric infection.
  • 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

  • Distinguish VPAC1 recruitment/support from VIPR2 IL-22 restraint.
  • 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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