Plasticity of innate lymphoid cell subsets
Citation
- Verified title: Plasticity of innate lymphoid cell subsets
- Publication year: 2020
- DOI: 10.1038/s41577-020-0282-9
- Metadata source: crossref-doi (confidence: high)
- Original local title: Plasticity of innate lymphoid cell subsets
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 subset plasticity
- Evidence profile: ILC subsets can shift transcriptional and cytokine programs in response to tissue and inflammatory cues.
- 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 #cell/ILC1 #cell/ILC2 #cell/ILC3 #outcome/inflammation #axis/ILC_plasticity #status/focused_crystallization
- Primary biological axis: ILC subsets can shift transcriptional and cytokine programs in response to tissue and inflammatory cues.
Why It Matters Here
This source adds ILC subset plasticity 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 frames ILC subset plasticity as a general feature of ILC biology.
- It is useful for interpreting ILC2-to-ILC1-like and ILC2/ILC3-like boundary states.
- It supports cautious state-based language rather than rigid subset-only interpretation.
- Use primary lung, nasal, or sputum sources for specific disease claims.
Claim-Level Confidence
- Medium-high confidence: ILC plasticity is a well-supported field concept.
- Medium confidence: review-level support should be paired with primary disease-context evidence.
Methods and Context
- Source-specific context: review-level synthesis of human and mouse ILC plasticity 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 use broad plasticity framing to erase marker, tissue, or disease-model boundaries.
- 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.
Related Pages
- ILC_in_lung_project
- ILC_in_lung
- ILC2
- ILC2 functional regulation mechanisms
- ILC2 roles in pulmonary disease
- Lung ILC Core Evidence Synthesis
- ILC Research Trend From Then To Now
- Reference coverage audit