Component

Mouse extrathymic regulatory T-cell differentiation after butyrate

Context-specific entity; species, compartment and exposure are stated on each claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. The rise in extrathymically generated Tregs after butyrate depended on the Foxp3 CNS1 enhancer in mice.

    Mouse Foxp3 CNS1 enhancer function → Mouse extrathymic regulatory T-cell differentiation after butyrate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse CNS1 genetic experiments.
    limitations
    Extrathymic differentiation is distinct from thymic Treg generation.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    An intact gene-regulatory element was needed for this differentiation response.
    primary_references
    Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24226773/ · DOI 10.1038/nature12726
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 342–348

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse CNS1 genetic experiments. · source_derived_draft · unverified_draft

    ## butyrate-cns1-dependency An intact gene-regulatory element was needed for this differentiation response. The rise in extrathymically generated Tregs after butyrate depended on the Foxp3 CNS1 enhancer in mice. Model: Mouse CNS1 genetic experiments. Limitations: Extrathymic differentiation is distinct from thymic Treg generation. Evidence access: Primary abstract Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24226773/ · DOI 10.1038/nature12726
    Complete structured claim and evidence

  2. The retinoic-acid-receptor antagonist LE135 abolished the increased Treg conversion induced by butyrate- or niacin-treated wild-type mouse dendritic cells.

    Mouse retinoic-acid-receptor signaling in butyrate/DC experiments; receptor subtype unresolved → Mouse extrathymic regulatory T-cell differentiation after butyrate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure S2I and methods
    experimental_model
    Mouse dendritic/T-cell coculture; LE135 1 micromolar.
    limitations
    Antagonist exposure is not a vitamin A withdrawal experiment; extra vitamin A was not demonstrated to improve a replete response.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Blocking vitamin A–related receptor signaling removed this immune-cell response.
    primary_references
    Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24412617/ · DOI 10.1016/j.immuni.2013.12.007
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 374–380

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dendritic/T-cell coculture; LE135 1 micromolar. · source_derived_draft · unverified_draft

    ## butyrate-retinoid-block Blocking vitamin A–related receptor signaling removed this immune-cell response. The retinoic-acid-receptor antagonist LE135 abolished the increased Treg conversion induced by butyrate- or niacin-treated wild-type mouse dendritic cells. Model: Mouse dendritic/T-cell coculture; LE135 1 micromolar. Limitations: Antagonist exposure is not a vitamin A withdrawal experiment; extra vitamin A was not demonstrated to improve a replete response. Evidence access: Primary full text, Figure S2I and methods Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24412617/ · DOI 10.1016/j.immuni.2013.12.007
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Butyrate increased histone H3 acetylation at Foxp3 regulatory regions under Treg-polarizing conditions and promoted Treg differentiation.

    Butyrate → Mouse regulatory T-cell transcription factor Foxp3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse naive T-cell differentiation, chromatin measurements and colitis experiments.
    limitations
    Not a claim that butyrate turns every T cell into a Treg or universally suppresses immunity. Correction record: Publisher correction reviewed: Figure 1d upper-right axis identifies Neuropilin-1-positive Foxp3-positive cells; the originally printed negative-marker label was wrong. The notice does not amend the Foxp3 histone-acetylation result cited here. https://www.nature.com/articles/nature13041
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The surrounding immune signals helped determine which gene program turned on.
    primary_references
    Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24226770/ · DOI 10.1038/nature12721

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 334–340

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse naive T-cell differentiation, chromatin measurements and colitis experiments. · source_derived_draft · unverified_draft

    ## butyrate-foxp3-acetylation The surrounding immune signals helped determine which gene program turned on. Butyrate increased histone H3 acetylation at Foxp3 regulatory regions under Treg-polarizing conditions and promoted Treg differentiation. Model: Mouse naive T-cell differentiation, chromatin measurements and colitis experiments. Limitations: Not a claim that butyrate turns every T cell into a Treg or universally suppresses immunity. Correction record: Publisher correction reviewed: Figure 1d upper-right axis identifies Neuropilin-1-positive Foxp3-positive cells; the originally printed negative-marker label was wrong. The notice does not amend the Foxp3 histone-acetylation result cited here. https://www.nature.com/articles/nature13041 Evidence access: Primary abstract Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24226770/ · DOI 10.1038/nature12721
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards