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Neuropeptide regulation of non-redundant ILC2 responses at barrier surfaces

Citation

  • Verified title: Neuropeptide regulation of non-redundant ILC2 responses at barrier surfaces
  • Publication year: 2022
  • DOI: 10.1038/s41586-022-05297-6
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Neuropeptide regulation of non-redundant ILC2 responses at barrier surfaces

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page was read beyond bulk registration and now records source-specific biological claims, model context, assay directness, and reuse boundaries.
  • Durable synthesis status: selected high-confidence claims from this source were propagated into ILC2 entity/topic/digest pages with source links.

Source Type

  • primary mouse and human barrier-surface neuroimmune ILC2 study
  • Evidence profile: Nmur1-driven genetic targeting, ILC2-specific amphiregulin deletion, anti-parasite and intestinal injury models, mouse/human NMU expression and ILC2 response assays.
  • Knowledge note status: focused source note suitable for wiki synthesis, with caveats preserved below.

Evidence Profile

  • Overall confidence: high for source-specific claims explicitly tied to the reported model, species, assay, and outcome; lower for cross-disease or human translation unless directly tested.
  • Evidence tags: #cell/ILC2 #tissue/lung #topic/regulation #topic/pulmonary_disease #axis/ILC2_niche #axis/interferon_brake #axis/type2_immunity #status/focused_crystallization
  • Primary biological axis: Although intestinal rather than lung-centered, this source is a high-value mechanism paper because it demonstrates non-redundant ILC2-derived AREG and conserved NMU responsiveness.

Why It Matters Here

Although intestinal rather than lung-centered, this source is a high-value mechanism paper because it demonstrates non-redundant ILC2-derived AREG and conserved NMU responsiveness.

Key Findings

  • Nmur1-based genetic targeting enables ILC2-specific perturbation in the presence of an intact adaptive immune system.
  • ILC2-derived amphiregulin has non-redundant roles in anti-parasite immunity and tissue protection after intestinal damage in the reported systems.
  • NMU is increased in inflamed mouse and human intestinal tissues and can induce AREG production by mouse and human ILC2s.
  • The source supports neuropeptide control of tissue-protective ILC2 output, but it should be used as barrier-surface mechanism evidence rather than direct lung disease proof.

Claim-Level Confidence

  • High confidence: ILC2-derived AREG is non-redundant in the reported intestinal barrier models.
  • High confidence: NMU can regulate AREG production by mouse and human ILC2s in the source-supported systems.
  • Medium confidence: lung relevance is mechanistic and comparative unless paired with lung NMU/NMUR1 sources.

Methods and Context

  • Species/context: mouse intestinal barrier models plus human intestinal tissue/cell evidence.
  • Assay directness: strong ILC2-specific genetic targeting and functional perturbation.
  • Best wiki use: non-redundant ILC2 function, AREG tissue protection, and conserved NMU responsiveness.

Caveats

  • This is not a primary lung disease paper; pair it with lung NMU/NMUR1 evidence before making pulmonary claims.
  • AREG repair biology should be curated separately from IL-5/IL-13 type 2 inflammation.

Contradiction and Supersession

  • Contradiction status: this source should be integrated as a context-specific branch, not as a universal statement about ILC2 biology.
  • Supersession status: this source refines earlier ILC2 models by adding spatial, interferon, neuroimmune, developmental, or type 2 framework detail; it does not supersede lung repair, allergic inflammation, or ILC2 plasticity branches.

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