ILC2s are the predominant source of intestinal ILC-derived IL-10

Citation

Verified title: ILC2s are the predominant source of intestinal ILC-derived IL-10
Publication year: 2020
DOI: 10.1084/jem.20191520
Metadata source: crossref-doi (confidence: high)
Original local title: ILC2s are the predominant source of intestinal ILC-derived IL-10

Ingest Mode

Mode: focused manual crystallization mode
Meaning: this source page has been manually reviewed for the adaptive-immunity follow-up question, including model system, tissue compartment, immune-cell target, assay directness, and claim-level boundaries.
Required boundary: reusable claims should preserve species, tissue, disease model, and whether evidence is primary perturbation, human association, ex vivo function, lineage taxonomy, or review-level synthesis.

Source Type

primary mouse intestinal ILC2 IL-10 study - Evidence profile: intestinal ILC-derived IL-10, ILC2 dominant source, regulatory cytokine output, gut inflammation/homeostasis context. - Knowledge note status: source-reviewed evidence note for gut-labeled ILC2 regulatory cytokine biology.

Evidence Profile

Overall confidence: medium-high for source-specific gut evidence that ILC2s are a dominant intestinal ILC-derived IL-10 source. - Evidence tags: #source/primary #species/mouse #tissue/gut #cell/ILC2 #cell/T_cell #assay/scRNAseq #assay/flow #assay/in_vivo #outcome/homeostasis #outcome/inflammation #axis/adaptive_immunity #axis/ILC_regulation #status/focused_crystallization - Primary biological axis: intestinal ILC2s can occupy an IL-10-producing regulatory state.

Why It Matters Here

This source adds an ILC2 regulatory/tolerance branch that is distinct from lung ILC2 OX40L costimulation and type 2 inflammation.

Key Findings

ILC2s were reported as the predominant source of intestinal ILC-derived IL-10 in the source context.
The source supports an ILC2 regulatory-cytokine state in gut, rather than only an IL-5/IL-13 effector model.
It is relevant to immune restraint and tolerance framing, but it is not direct lung evidence.
T-cell implications should be described cautiously unless source-specific functional assays are cited.

Claim-Level Confidence

Medium-high confidence: gut ILC2s can be a dominant ILC-derived IL-10 source in the reported system.
Medium confidence: this supports ILC2 regulatory-state framing.
Low confidence: lung ILC2 IL-10 or direct Treg control should not be inferred without lung data.

Methods and Context

Species/context: mouse intestinal ILC profiling and functional context.
Compartment: gut.
Assay directness: strong for ILC-derived IL-10 source assignment; indirect for lung adaptive immunity.
Best wiki use: ILC2 regulatory cytokine branch.

Caveats

Keep gut context explicit.
Do not treat IL-10+ ILC2s as a default lung ILC2 state.
Separate cytokine restraint from direct adaptive-cell control.

Contradiction and Supersession

Contradiction status: complements type 2 effector ILC2 literature by adding regulatory cytokine output.
Supersession status: not superseded.