ILC3s sense gut microbiota through STING to initiate immune tolerance

Citation

Verified title: ILC3s sense gut microbiota through STING to initiate immune tolerance
Publication year: 2025
DOI: 10.1016/j.immuni.2025.05.016
Metadata source: crossref-doi (confidence: high)
Original local title: ILC3s sense gut microbiota through STING to initiate immune tolerance

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 gut ILC3-STING-Treg tolerance study - Evidence profile: ILC3 microbiota sensing, STING signaling, CCR7-dependent migration to gut-draining lymph nodes, antigen-presentation signatures, microbiota-specific Tregs, and chronic inflammation restraint. - Knowledge note status: source-reviewed evidence note for gut ILC3 innate-sensing-to-adaptive-tolerance axis.

Evidence Profile

Overall confidence: high for source-specific gut evidence that ILC3-intrinsic STING supports microbiota-specific Treg instruction and inflammatory restraint. - Evidence tags: #source/primary #species/mouse #species/human #tissue/gut #cell/ILC3 #cell/Treg #cell/T_cell #assay/scRNAseq #assay/RNAseq #assay/in_vivo #assay/KO #outcome/homeostasis #outcome/inflammation #axis/adaptive_immunity #axis/ILC_regulation #status/focused_crystallization - Primary biological axis: ILC3 STING links microbial sensing, lymph-node migration, antigen-presentation programs, and microbiota-specific Treg tolerance.

Why It Matters Here

This recent source adds an upstream sensing mechanism to the ILC3-Treg tolerance model: microbiota-derived signals can be read through ILC3 STING.

Key Findings

ILC3s were described as RORgammat-positive antigen-presenting cells that sense microbiota through STING in the reported gut context.
ILC3-intrinsic STING enhanced CCR7-dependent migration to gut-draining lymph nodes.
STING signaling supported microbiota-specific regulatory T-cell instruction and restrained chronic inflammation.
Uncontrolled inflammatory context depleted tissue-protective ILC3s, adding a disease-state caveat.

Claim-Level Confidence

High confidence: gut ILC3 STING supports microbiota-specific Treg tolerance in the reported source.
Medium-high confidence: STING belongs in the ILC3 adaptive-tolerance mechanism map.
Low confidence: lung ILC3 STING-Treg claims require pulmonary evidence.

Methods and Context

Species/context: gut microbiota and inflammatory tolerance models with human relevance context.
Compartment: gut and gut-draining lymph nodes.
Assay directness: strong for gut tolerance axis; indirect for lung.
Best wiki use: ILC3 sensing-to-Treg pathway.

Caveats

Keep gut and lymph-node context explicit.
Do not treat STING as universally protective; inflammatory context can change ILC3 fate.
Avoid direct pulmonary extrapolation.

Contradiction and Supersession

Contradiction status: adds a sensing/migration layer to earlier MHCII/Treg selection sources.
Supersession status: recent extension, not replacement.