Component

IL-2

The cytokine output at the end of the featured pathway.

4 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 it acts on

  1. IL-2 signaling activates STAT5 in the studied CD4 T-cell differentiation context.

    IL-2 → STAT5 source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    antigen-specific CD4 T cells
    experimental_model
    LCMV infection and signaling perturbations
    limitations
    No selenium intervention in this study.
    organism
    mouse

    Selenium: literature corrections and mechanism additions · lines 918–928

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · LCMV infection and signaling perturbations · secondary_verified · secondary_verified

    ## il2-activates-stat5-tfh-context IL-2 engages a signal that can oppose Tfh development. IL-2 signaling activates STAT5 in the studied CD4 T-cell differentiation context. Organism: mouse Cell type: antigen-specific CD4 T cells Experimental model: LCMV infection and signaling perturbations Limitations: No selenium intervention in this study. Primary reference: [STAT5 is a potent negative regulator of TFH cell differentiation](https://pmc.ncbi.nlm.nih.gov/articles/PMC3281266/)
    Complete structured claim and evidence

What acts on it

  1. IL-2 production declined during depletion; immune indices returned to baseline after the third repletion stage.

    Vitamin B6 → IL-2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Eight healthy older adults in sequential dietary depletion and repletion experiment.
    exposure
    Depletion up to 20 days, then three 21-day repletion stages; final short 50 mg/day phase. Repletion-stage intakes are historical experimental context.
    limitations
    Recovery occurred during a sequence of increasing intakes; no universal individual requirement or treatment dose follows.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The observed immune changes were reversible with restored intake.
    primary_references
    [b6-meydani1991] Vitamin B-6 deficiency impairs interleukin 2 production and lymphocyte proliferation in elderly adults (1991). https://pubmed.ncbi.nlm.nih.gov/2021134/ DOI: 10.1093/ajcn/53.5.1275
    tissue_or_cell_type
    Ex-vivo human immune-cell assays
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1681–1691

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eight healthy older adults in sequential dietary depletion and repletion experiment. · source_derived_draft · unverified_draft

    ### b6-depletion-il2 IL-2 production declined during depletion; immune indices returned to baseline after the third repletion stage. Condition category: nutrient_deficiency nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The observed immune changes were reversible with restored intake. organism: Homo sapiens tissue_or_cell_type: Ex-vivo human immune-cell assays experimental_model: Eight healthy older adults in sequential dietary depletion and repletion experiment. limitations: Recovery occurred during a sequence of increasing intakes; no universal individual requirement or treatment dose follows. exposure: Depletion up to 20 days, then three 21-day repletion stages; final short 50 mg/day phase. Repletion-stage intakes are historical experimental context. [b6-meydani1991] Vitamin B-6 deficiency impairs interleukin 2 production and lymphocyte proliferation in elderly adults (1991). https://pubmed.ncbi.nlm.nih.gov/2021134/ DOI: 10.1093/ajcn/53.5.1275
    Complete structured claim and evidence

  2. IL2 transcription produces IL-2 protein.

    IL2 transcription → IL-2 source_derived_draftsupplied_source_only
    Experimental context and source evidence
    cell_type
    · T cell
    evidence_scope
    Source-derived draft; primary-source verification required
    organism
    · Human

    Selenium in immune cells · lines 30–38

    Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft

    5. TCR → LCK → ZAP70 → LAT → PLCγ1 → PIP₂ → IP₃ + DAG 6. IP₃ → IP3R → ER Ca²⁺ release → store depletion 7. STIM1 oligomerizes → ORAI1 → CRAC channel → sustained Ca²⁺ entry 8. Ca²⁺/calmodulin → CALCINEURIN (PP2B) → dephosphorylates NFAT 9. NFAT → nucleus → partners with AP-1 → IL2, IFNG, CD25 transcription
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Experimental human zinc restriction reduced interleukin-2 production, contributing to the selective decline in the tested TH1-associated cytokine response.

    Zinc → T-cell interleukin-2 production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    interleukin-2 (measured_cytokine)
    evidence_location
    Indexed primary abstract.
    evidence_span
    {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106}
    experimental_model
    Experimental dietary zinc restriction and repletion in humans
    exposure
    Baseline, end of zinc restriction, and following repletion were assessed.
    limitations
    Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    Zinc shortage reduced interleukin-2 production in the tested immune cells.
    primary_references
    [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002
    tissue_or_cell_type
    T lymphocytes and cytokine production
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1362–1375

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental dietary zinc restriction and repletion in humans · source_derived_draft · unverified_draft

    ### zn-clin-depletion-il2 Experimental human zinc restriction reduced interleukin-2 production, contributing to the selective decline in the tested TH1-associated cytokine response. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage reduced interleukin-2 production in the tested immune cells. organism: Homo sapiens tissue_or_cell_type: T lymphocytes and cytokine production experimental_model: Experimental dietary zinc restriction and repletion in humans limitations: Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk. exposure: Baseline, end of zinc restriction, and following repletion were assessed. cross_nutrient: interleukin-2 (measured_cytokine) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106} [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002
    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