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Metabolic features of innate lymphoid cells

Citation

  • Verified title: Metabolic features of innate lymphoid cells
  • Publication year: 2022
  • DOI: 10.1084/jem.20221140
  • Metadata source: crossref-doi (confidence: high)
  • Original local title: Metabolic features of innate lymphoid cells

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page has been manually reviewed for the ILC2 regulatory-context question, including tissue compartment, model system, regulatory mediator, assay directness, and whether the source is primary or review-level evidence.
  • Required boundary: reusable claims should preserve species, tissue, mediator, disease model, and whether evidence is primary perturbation or review-level synthesis.

Source Type

  • review on ILC metabolic regulation
  • Evidence profile: ILC function depends on metabolic adaptability shaped by tissue environment, activation state, and disease context.
  • Knowledge note status: source-reviewed evidence note suitable for ILC2 regulation context.

Evidence Profile

  • Overall confidence: source-specific confidence is assigned to the biological claim below, not to PDF processing.
  • Evidence tags: #source/review #species/human #species/mouse #tissue/lung #tissue/gut #tissue/skin #cell/ILC1 #cell/ILC2 #cell/ILC3 #axis/metabolism #axis/ILC_regulation #outcome/homeostasis #outcome/inflammation #status/focused_crystallization
  • Primary biological axis: ILC function depends on metabolic adaptability shaped by tissue environment, activation state, and disease context.

Why It Matters Here

This source adds metabolic features of ILCs review to the ILC2 regulatory map. Its durable use depends on tissue and source-type boundaries: primary studies can support source-specific mechanisms, while reviews should orient interpretation and point to primary anchors.

Key Findings

  • The review highlights metabolic adaptability as a central feature of ILC activation and function.
  • It is useful for placing autophagy, glycolysis, OXPHOS, lipid handling, mTOR, and tissue nutrient cues into one regulatory layer.
  • It should be treated as overview context rather than primary evidence for a specific metabolic perturbation.
  • Use primary source pages for autophagy, human ILC2 metabolism, HIF-1alpha/glycolysis, dopamine-mitochondrial activity, and ILC3 CD71-iron claims.

Claim-Level Confidence

  • Medium confidence: useful review-level metabolic framework for ILC biology.
  • Low confidence: individual pathway causality should be sourced to primary studies.

Methods and Context

  • Source-specific context: review-level synthesis of ILC metabolism literature.
  • Best wiki use: ILC2 functional regulation, tissue-context guardrails, and source routing.
  • Assay directness: strongest for the source tissue/model; indirect for lung disease unless lung data are present.

Caveats

  • Do not collapse all ILC metabolic pathways into a single universal mechanism.
  • Preserve species, tissue compartment, mediator, and disease-model labels.
  • Reviews should frame the field; primary sources should anchor causal claims.

Contradiction and Supersession

  • Contradiction status: complements the current ILC2 regulatory map by adding tissue-context, developmental, metabolic, neuroimmune, epithelial, or therapeutic framing.
  • Supersession status: not superseded; use alongside direct pulmonary ILC2 sources with explicit evidence labels.

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