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Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity

Citation

  • Verified title: Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity
  • Publication year: 2016
  • DOI: 10.1016/j.jaci.2016.03.019
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity

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 mouse allergic-airway disease study
  • crystallization status: manually promoted into focused manual crystallization batch 3
  • Batch 3 axis: ILC2/ILC3 obesity-associated allergic airway disease

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: mouse high-fat diet obesity plus allergic airway inflammation; lung ILC2/ILC3 enumeration and cytokine-associated disease readouts.
  • Batch 3 synthesis role: ILC2/ILC3 obesity-associated allergic airway disease.

Why It Matters Here

This source links metabolic disease context to lung allergic inflammation and places both ILC2s and ILC3s in obesity-exacerbated AHR rather than treating asthma as only a lean type 2 model.

Key Findings

  • High-fat diet-induced obesity exacerbated allergic airway inflammatory features, including eosinophilia and AHR, in the reported mouse model.
  • The source text reports increased total and cytokine-expressing lung ILC2s and ILC3s in obese allergic airway disease compared with lean allergic controls.
  • The paper supports obesity as a context that can reshape innate lymphoid contributions to allergic airway disease.
  • This should be curated as mouse metabolic-asthma evidence, not as a direct human obesity-asthma causal claim.

Claim-Level Confidence

  • High confidence: this source supports a mouse-model link between HFD-induced obesity, worsened allergic airway disease, and altered lung ILC2/ILC3 responses.
  • Medium-high confidence: the source supports ILC2/ILC3 involvement in obesity-exacerbated allergic inflammation, but exact mediator hierarchy should be checked against figures before detailed reuse.
  • Low confidence: broad extrapolation to human obesity-associated asthma phenotypes is not justified without human cohort evidence.

Methods and Context

  • Source kind inferred from title/tags/text: primary research article with animal-model evidence.
  • Species or sample frame detected: human, mouse
  • Tissue or disease context detected: lung/airway, asthma/allergy, nasal polyp
  • Assay modalities detected from tags: single-cell RNA-seq
  • 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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