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Characterization and Quantification of Innate Lymphoid Cell Subsets in Human Lung

Citation

  • Verified title: Characterization and Quantification of Innate Lymphoid Cell Subsets in Human Lung
  • Publication year: 2016
  • DOI: 10.1371/journal.pone.0145961
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Characterization and Quantification of Innate Lymphoid Cell Subsets in Human Lung

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page has been manually upgraded for a priority crystallization pass and may support durable topic/entity/project/digest synthesis.
  • Required boundary: reusable claims from this source still need source-linked species, tissue, assay, model, and confidence labels.

Source Type

  • primary human lung flow-cytometry study
  • human lung ILC1, ILC2, NCR+ ILC3, and NCR- ILC3 subset baseline source
  • COPD comparison source with small sample size and trend-level disease signal
  • crystallization status: manually promoted into batch 2 high-priority lung ILC source note

Evidence Profile

  • Overall confidence: high for presence and flow-cytometric discrimination of major ILC subsets in human lung tissue.
  • Directness to this project: very high for human lung ILC entity anchoring; medium for COPD disease interpretation because COPD shifts were described as tendencies and sample size was limited.
  • Evidence type: human lung surgical tissue, multi-color flow cytometry, surface-marker and transcription-factor-based subset definition, ex vivo cytokine staining after stimulation.
  • Main biological axis: human lung CD45+ Lin- CD127+ ILCs -> ILC1/ILC2/ILC3 subset discrimination -> IFN-gamma, IL-5, IL-17A, IL-22, GM-CSF functional potential.

Why It Matters Here

This is the key human-lung baseline source for the entity pages. It prevents the wiki from relying only on mouse asthma or infection models by showing that ILC1, ILC2, and ILC3 subsets can be detected and functionally profiled in human lung tissue.

Key Findings

  • The study identified ILC1, ILC2, and ILC3 subsets within CD45+ Lin- CD127+ pulmonary ILCs in human lung tissue.
  • ILC1, ILC2, and ILC3 assignments were supported by surface markers including IL12Rbeta2, CRTH2, CD117, and NKp44, plus transcription factors T-bet, GATA-3, and RORgammat.
  • Human pulmonary ILCs showed induced signature cytokine potential, including IFN-gamma, IL-5, IL-17A, IL-22, and GM-CSF.
  • COPD lungs showed a tendency toward higher NCR- ILC3 frequency and increased IL-17A/IL-22-expressing ILCs, but the source text notes limited patient numbers and trend-level interpretation.

Claim-Level Confidence

  • High confidence: human lung tissue contains flow-defined ILC1, ILC2, and ILC3 subsets, including NCR+ and NCR- ILC3 compartments.
  • High confidence: human pulmonary ILCs can express subset-associated cytokines after stimulation in this study.
  • Medium confidence: COPD may be associated with a shift toward NCR- ILC3 and IL-17A/IL-22-positive ILCs, but this should be treated as trend-level because of limited sample size.
  • Low confidence: this source alone does not establish causal ILC mechanisms in COPD progression or exacerbation.

Methods and Context

  • Human lung tissue from surgical lung resections, including controls and COPD GOLD I/II subjects.
  • Flow cytometry on single-cell lung suspensions with FMO-supported gating.
  • ILC subset definitions include CD45, lineage exclusion, CD127, IL12Rbeta2, CRTH2, CD117, and NKp44.
  • Functional cytokine potential assessed after PMA/ionomycin stimulation rather than direct in vivo secretion.

Caveats

  • COPD claims are associative and trend-level, not mechanistic.
  • Surgical lung tissue and digestion can affect rare-cell recovery and subset proportions.
  • Marker definitions reflect the study's flow panel and should be compared carefully with modern scRNA-seq or CyTOF definitions.

Contradiction and Supersession

  • Contradiction/tension: supports human lung ILC3 presence and possible COPD skewing, but stronger COPD plasticity claims require the Silver et al. COPD-trigger paper.
  • Supersession status: not superseded; this source is best used as a human lung baseline anchor.

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