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Adventitial Stromal Cells Define Group 2 Innate Lymphoid Cell Tissue Niches

Citation

  • Verified title: Adventitial Stromal Cells Define Group 2 Innate Lymphoid Cell Tissue Niches
  • Publication year: 2019
  • DOI: 10.1016/j.immuni.2019.02.002
  • Metadata source: pubmed (confidence: high)
  • Original local title: Adventitial Stromal Cells Define Group 2 Innate Lymphoid Cell Tissue Niches

Ingest Mode

  • Mode: focused manual crystallization mode
  • Meaning: this source page was read beyond bulk registration and now records source-specific biological claims, model context, assay directness, and reuse boundaries.
  • Durable synthesis status: selected high-confidence claims from this source were propagated into ILC2 entity/topic/digest pages with source links.

Source Type

  • primary mouse tissue-imaging and stromal-niche study
  • Evidence profile: quantitative 3D imaging, flow cytometry, scRNA-seq, stromal-cell functional assays, helminth/type 2 perturbation, and ASC depletion in mouse lung and other tissues.
  • Knowledge note status: focused source note suitable for wiki synthesis, with caveats preserved below.

Evidence Profile

  • Overall confidence: high for source-specific claims explicitly tied to the reported model, species, assay, and outcome; lower for cross-disease or human translation unless directly tested.
  • Evidence tags: #cell/ILC2 #tissue/lung #topic/regulation #topic/pulmonary_disease #axis/ILC2_niche #axis/interferon_brake #axis/type2_immunity #status/focused_crystallization
  • Primary biological axis: This paper gives the wiki a spatial organizing principle for lung ILC2 biology: ILC2s are not only cytokine-responsive cells, but tissue-positioned lymphocytes embedded in adventitial stromal niches.

Why It Matters Here

This paper gives the wiki a spatial organizing principle for lung ILC2 biology: ILC2s are not only cytokine-responsive cells, but tissue-positioned lymphocytes embedded in adventitial stromal niches.

Key Findings

  • ILC2s localize in a conserved adventitial niche around lung bronchi and larger vessels rather than being randomly distributed through lung tissue.
  • ILC2s are closely associated with fibroblast-like adventitial stromal cells (ASCs) that express IL-33 and TSLP.
  • ASC-derived TSLP supports ILC2 accumulation and activation in vitro, and ASC-derived IL-33 contributes to type 2 lymphocyte accumulation and function during helminth-driven lung inflammation.
  • ILC2s and IL-13 reciprocally promote ASC expansion and IL-33 expression, supporting a stromal-immune feedback loop.

Claim-Level Confidence

  • High confidence: mouse lung ILC2s occupy adventitial/peribronchovascular niches and are anatomically associated with IL-33/TSLP-expressing ASCs.
  • High confidence: the source supports a reciprocal ASC-ILC2-IL-13 circuit in type 2 inflammation.
  • Medium confidence: human or disease-general claims should be treated as conceptual extension unless matched human lung spatial evidence is available.

Methods and Context

  • Species/context: mouse lung and multiple tissues, with helminth/type 2 immune perturbation.
  • Assay directness: strong spatial and perturbation evidence for niche localization and stromal support.
  • Best wiki use: tissue niche, stromal IL-33/TSLP, reciprocal ILC2-stromal feedback, and interpretation of lung ILC2 position.

Caveats

  • Do not treat adventitial niche localization as proof that every disease-relevant ILC2 remains in that niche during inflammation.
  • Separate ASC-derived IL-33/TSLP support from epithelial alarmin release; both can regulate ILC2s but represent different tissue layers.

Contradiction and Supersession

  • Contradiction status: this source should be integrated as a context-specific branch, not as a universal statement about ILC2 biology.
  • Supersession status: this source refines earlier ILC2 models by adding spatial, interferon, neuroimmune, developmental, or type 2 framework detail; it does not supersede lung repair, allergic inflammation, or ILC2 plasticity branches.

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