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Tissue signals imprint ILC2 identity with anticipatory function

Citation

  • Verified title: Tissue signals imprint ILC2 identity with anticipatory function
  • Publication year: 2018
  • DOI: 10.1038/s41590-018-0201-4
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Tissue signals imprint ILC2 identity with anticipatory function

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 tissue-imprinting ILC2 study
  • crystallization status: manually promoted into focused manual crystallization batch 3
  • Batch 3 axis: tissue imprinting of ILC2 identity

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: multi-tissue mouse and human ILC2 transcriptional comparison; epithelial cytokine deficiency; IL-33/IL-25/TSLP and IL-18 context.
  • Batch 3 synthesis role: tissue imprinting of ILC2 identity.

Why It Matters Here

This source supports the principle that lung ILC2s carry tissue-specific identities before disease challenge.

Key Findings

  • The source reports that transcriptional profiling groups ILC2s by tissue of origin.
  • Tissue-specific ILC2 identity persists even when common epithelial cytokine signaling is perturbed in the reported system.
  • IL-5+ ILC2 homeostatic cytokine output depends on IL-33/IL-25/TSLP signaling, while other tissue-imprinted signatures remain distinct.
  • The source supports tissue imprinting and anticipatory function as core ILC2 interpretive principles.

Claim-Level Confidence

  • High confidence: ILC2 identity is tissue-imprinted in the reported mouse and human comparative systems.
  • Medium-high confidence: lung ILC2 interpretation should preserve tissue-of-origin labels, but disease-specific causal roles require separate disease sources.
  • Low confidence: tissue-imprinting data do not by themselves establish asthma mechanism.

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: gut/intestine, skin
  • 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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