WASH maintains NKp46+ ILC3 cells by promoting AHR expression

Citation

Verified title: WASH maintains NKp46+ ILC3 cells by promoting AHR expression
Publication year: 2017
DOI: 10.1038/ncomms15685
Metadata source: crossref-doi (confidence: high)
Original local title: WASH maintains NKp46+ ILC3 cells by promoting AHR expression

Ingest Mode

Mode: focused manual crystallization mode
Meaning: this source page was manually upgraded and now supports source-linked WASH-AHR maintenance claims for ILC3s.
Durable synthesis status: selected high-confidence identity-maintenance claims from this source were propagated into ILC3 entity and mechanism pages.

Source Type

primary mouse intestinal NKp46-positive ILC3 maintenance study
Evidence profile: WASH expression in ILC3s, Arid1a recruitment to the Ahr promoter, perturbation of the WASH-Arid1a axis, and subset-maintenance outcomes
Knowledge note status: focused source note suitable for mechanistic ILC3 identity maintenance, with gut-context labeling

Evidence Profile

Overall confidence: high for source-specific claims that WASH maintains NKp46-positive ILC3s by supporting AHR expression in the reported system.
Evidence tags: #cell/ILC3 #tissue/gut #topic/regulation #axis/AHR #axis/chromatin_regulation #axis/identity_control #status/focused_crystallization
Primary biological axis: WASH promotes maintenance of the NKp46-positive ILC3 branch through Arid1a-associated activation of Ahr transcription.

Why It Matters Here

This paper is helpful because it takes the broad AHR theme and makes it mechanistically sharper. Instead of saying only that AHR matters, it identifies an upstream chromatin-regulatory pathway that helps sustain an ILC3 identity program.

Key Findings

WASH was highly expressed in the nucleus of ILC3s in the reported system.
In NKp46-positive ILC3s, WASH recruited Arid1a to the Ahr promoter and thereby supported AHR expression.
Loss of Arid1a impaired AHR expression and reduced maintenance of NKp46-positive ILC3s.
The source therefore places WASH upstream of an AHR-centered maintenance program rather than treating AHR as an isolated endpoint.
This is especially useful for the wiki because it adds a chromatin-regulation branch to the ILC3 identity map.

Claim-Level Confidence

High confidence: WASH promotes maintenance of NKp46-positive ILC3s in the reported mouse system.
High confidence: the mechanism is linked to Arid1a recruitment at the Ahr promoter and preservation of AHR expression.
Medium-high confidence: this source strengthens the broader claim that AHR-centered ILC3 maintenance is under upstream epigenetic or chromatin control.
Low confidence: this paper should not be used as direct evidence for pulmonary NKp46-positive ILC3 biology without matched lung data.

Methods and Context

Species/context: mouse gut ILC3 subset biology with a specific focus on the NKp46-positive branch.
Assay directness: strong for the WASH-Arid1a-AHR mechanism and subset-maintenance consequence.
Best wiki use: ILC3 identity maintenance, AHR-upstream regulation, and chromatin-level mechanism context.

Caveats

This is a gut-centered mechanistic paper and should stay explicitly labeled as such.
The main supported claim is about the NKp46-positive ILC3 branch, not every ILC3 subset equally.
It is best used to enrich regulation logic rather than to claim direct lung pathology.

Contradiction and Supersession

Contradiction status: this source deepens, rather than contradicts, the foundational AHR literature by providing an upstream maintenance mechanism.
Supersession status: not superseded; it remains a strong mechanistic companion to AHR-centered ILC3 identity papers.