Component

T helper 17 cell

T helper 17 cell; state and tissue specified by each experiment.

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

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

Where it participates (unsigned role)

  1. Epithelial Rarb deletion reduced intestinal Th17 IL-17A production without reducing overall Th17 frequency.

    Retinoic acid receptor beta → Interleukin 17A source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_locator
    Figure 4A-D
    experimental_model
    Mouse MODE-K cells and intestinal epithelial Rarb deletion.
    exposure
    Epithelial Rarb deletion
    limitations
    Does not establish a complete retinol-transfer chain.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    A receptor in epithelial cells helps neighboring immune cells function.
    primary_references
    [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    tissue_or_cell_type
    Intestinal lamina propria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1331–1342

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse MODE-K cells and intestinal epithelial Rarb deletion. · source_derived_draft · unverified_draft

    ### va-sig-rarb-th17-effector Epithelial Rarb deletion reduced intestinal Th17 IL-17A production without reducing overall Th17 frequency. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor in epithelial cells helps neighboring immune cells function. organism: Mus musculus tissue_or_cell_type: Intestinal lamina propria experimental_model: Mouse MODE-K cells and intestinal epithelial Rarb deletion. limitations: Does not establish a complete retinol-transfer chain. evidence_locator: Figure 4A-D exposure: Epithelial Rarb deletion [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    Complete structured claim and evidence
  2. Recombinant SAA1 restored impaired Th17 cytokine output in cultured lamina propria cells from epithelial Rarb mutants.

    Serum amyloid A1 → Interleukin 17A source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_locator
    Figure 4E
    experimental_model
    Mouse MODE-K cells and intestinal epithelial Rarb deletion.
    exposure
    rSAA1 during 4-hour stimulation
    limitations
    Rescue does not establish delivery of retinol to Th17 cells.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Adding an epithelial-associated mediator rescued the measured immune output.
    primary_references
    [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    tissue_or_cell_type
    Ex vivo intestinal lamina propria cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1344–1355

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse MODE-K cells and intestinal epithelial Rarb deletion. · source_derived_draft · unverified_draft

    ### va-sig-saa1-rescue-th17 Recombinant SAA1 restored impaired Th17 cytokine output in cultured lamina propria cells from epithelial Rarb mutants. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding an epithelial-associated mediator rescued the measured immune output. organism: Mus musculus tissue_or_cell_type: Ex vivo intestinal lamina propria cells experimental_model: Mouse MODE-K cells and intestinal epithelial Rarb deletion. limitations: Rescue does not establish delivery of retinol to Th17 cells. evidence_locator: Figure 4E exposure: rSAA1 during 4-hour stimulation [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    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