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Microbiota-Dependent Crosstalk Between Macrophages and ILC3 Promotes Intestinal Homeostasis

Citation

  • Verified title: Microbiota-Dependent Crosstalk Between Macrophages and ILC3 Promotes Intestinal Homeostasis
  • Publication year: 2014
  • DOI: 10.1126/science.1249288
  • Metadata source: crossref-title (confidence: high)
  • Original local title: Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page has been manually reviewed for the adaptive-immunity follow-up question, including model system, tissue compartment, immune-cell target, assay directness, and claim-level boundaries.
  • Required boundary: reusable claims should preserve species, tissue, disease model, and whether evidence is primary perturbation, human association, ex vivo function, lineage taxonomy, or review-level synthesis.

Source Type

primary gut ILC3-myeloid tolerance study - Evidence profile: microbiota-dependent macrophage-ILC3 crosstalk, ILC3-derived GM-CSF/CSF2, myeloid regulatory function, Treg-supportive intestinal homeostasis. - Knowledge note status: source-reviewed evidence note for gut-labeled indirect ILC3 support of adaptive tolerance.

Evidence Profile

Overall confidence: high for source-specific gut evidence that microbiota-conditioned ILC3-myeloid crosstalk supports intestinal regulatory homeostasis. - Evidence tags: #source/primary #species/mouse #tissue/gut #cell/ILC3 #cell/macrophage #cell/Treg #assay/in_vivo #assay/flow #outcome/homeostasis #outcome/inflammation #axis/adaptive_immunity #axis/ILC_regulation #status/focused_crystallization - Primary biological axis: microbiota signals promote an ILC3-GM-CSF-myeloid circuit that supports regulatory intestinal immunity.

Why It Matters Here

This source adds an indirect adaptive-immunity branch: ILC3s can support Treg-permissive tolerance through myeloid intermediates rather than only through direct T-cell contact.

Key Findings

  • Microbiota-dependent ILC3-macrophage crosstalk promotes intestinal homeostasis in the reported system.
  • ILC3-derived GM-CSF/CSF2 supports mononuclear phagocyte regulatory function.
  • The regulatory myeloid output is relevant to Treg-associated tolerance, but the ILC3-to-Treg link is indirect.
  • The source should remain gut-labeled and should not be used as pulmonary macrophage or lung Treg causality.

Claim-Level Confidence

  • High confidence: gut ILC3-myeloid crosstalk supports intestinal regulatory homeostasis in the reported model.
  • Medium-high confidence: this source supports an indirect ILC3-myeloid-Treg tolerance pathway.
  • Low confidence: direct lung Treg or lung macrophage claims are not justified from this source alone.

Methods and Context

  • Species/context: mouse gut microbiota and intestinal homeostasis models.
  • Compartment: intestine.
  • Assay directness: strong for gut ILC3-myeloid regulatory crosstalk; indirect for lung and for direct ILC3-Treg contact.
  • Best wiki use: indirect adaptive tolerance context.

Caveats

  • Preserve the myeloid intermediate.
  • Keep gut context explicit.
  • Do not collapse GM-CSF-driven myeloid regulation with direct ILC3-MHCII T-cell selection.

Contradiction and Supersession

  • Contradiction status: complements direct ILC3-T-cell/Treg sources by adding a myeloid intermediary.
  • Supersession status: not superseded.

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