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The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Citation

  • Verified title: The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation
  • Publication year: 2017
  • DOI: 10.1038/nature24029
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page was upgraded during focused manual crystallization batch 3 and can support durable synthesis when claims stay source-linked.
  • Required boundary: preserve species, tissue, assay, model, perturbation, and confidence labels when reusing claims.

Source Type

  • primary neuroimmune ILC2 allergic lung inflammation study
  • crystallization status: manually promoted into focused manual crystallization batch 3
  • Batch 3 axis: NMU/NMUR1 amplification of ILC2 allergic lung inflammation

Evidence Profile

  • Overall confidence: medium-high to high for the source-specific claims listed below; lower for broad extrapolation beyond the reported system.
  • Evidence profile: single-cell/transcriptomic ILC2 states, NMUR1 expression, NMU stimulation, IL-25/IL-33 alarmin context, allergen challenge.
  • Batch 3 synthesis role: NMU/NMUR1 amplification of ILC2 allergic lung inflammation.

Why It Matters Here

This source is a foundational mouse neuroimmune ILC2 paper and pairs with the newer human NMU/NMUR1 asthma evidence.

Key Findings

  • The source reports that Nmur1 is preferentially expressed by ILC2s at steady state and after IL-25 stimulation.
  • NMU activates ILC2s in vitro and co-administration with IL-25 amplifies allergic inflammation in vivo.
  • Loss of NMU-NMUR1 signaling reduces ILC2 frequency and effector function after allergen challenge.
  • This paper establishes neuroimmune amplification as a core ILC2 regulatory branch.

Claim-Level Confidence

  • High confidence: NMU-NMUR1 signaling amplifies ILC2-driven allergic lung inflammation in the reported mouse systems.
  • Medium-high confidence: together with human airway NMUR1 evidence, this supports a conserved neuroimmune axis, but compartment and phenotype boundaries remain important.
  • Low confidence: NMU should not be treated as universally activating for all ILC2 states without context.

Methods and Context

  • Source kind inferred from title/tags/text: primary or literature research article.
  • Species or sample frame detected: mouse
  • Tissue or disease context detected: lung/airway, asthma/allergy, nervous system
  • Assay modalities detected from tags: flow cytometry, single-cell RNA-seq, RNA-seq, in vivo model, in vitro assay, genetic or knockout perturbation
  • Use this source page as a knowledge-oriented first pass; confirm experimental design, gating, perturbation, and outcome measures before manuscript-level use.

Caveats

  • This batch crystallization used source text and extracted article context to promote source-specific claims, but detailed figure panels should still be checked before manuscript-level quotation.
  • Preserve disease, tissue, species, and assay boundaries when reusing this source.
  • Do not use this source alone to make broad pan-ILC, pan-asthma, or clinical-treatment claims.

Contradiction and Supersession

  • Contradiction status: not assessed during bulk ingestion.
  • Supersession status: not assessed during bulk ingestion.

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