Component

Interleukin 10

Interleukin 10; read each linked claim for the measured context and model.

2 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

Where it participates (unsigned role)

  1. We identify the metabolite and neurotransmitter GABA as a candidate signalling molecule synthesized and secreted by activated B cells and plasma cells, B cell-derived GABA promotes monocyte differentiation into anti-inflammatory macrophages that secrete interleukin-10 and inhibit CD8-positive T cell killer function, and in mice B cell deficiency or B cell-specific inactivation of the GABA-generating enzyme GAD67 enhances anti-tumour responses.

    B cell → Gamma-aminobutyric acid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/34732892.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b", "start_char": 0, "end_char": 878, "text_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b"}
    experimental_model
    Identification of a metabolite secreted by activated B cells, with monocyte differentiation and two genetic tests in mice
    exposure
    B cell-derived GABA, with B cell deficiency and B cell-specific inactivation of the GABA-generating enzyme GAD67
    limitations
    The B cell-specific enzyme deletion is what makes the source assignment strong. The enzyme deleted is GAD67, not the GAD65 that is the diabetes autoantigen.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Mouse
    plain_language
    B cells release this molecule into a tumour, where it turns arriving monocytes into cells that shut down the killers.
    primary_references
    [gb-p34732892] B cell-derived GABA elicits IL-10+ macrophages to limit anti-tumour immunity. (2021). https://pubmed.ncbi.nlm.nih.gov/34732892/ DOI: 10.1038/s41586-021-04082-1
    tissue_or_cell_type
    B cell, monocyte and tumour

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 599–610

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Identification of a metabolite secreted by activated B cells, with monocyte differentiation and two genetic tests in mice · source_derived_draft · unverified_draft

    ### gb-b-cells-secrete-gaba-that-shields-tumours We identify the metabolite and neurotransmitter GABA as a candidate signalling molecule synthesized and secreted by activated B cells and plasma cells, B cell-derived GABA promotes monocyte differentiation into anti-inflammatory macrophages that secrete interleukin-10 and inhibit CD8-positive T cell killer function, and in mice B cell deficiency or B cell-specific inactivation of the GABA-generating enzyme GAD67 enhances anti-tumour responses. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: B cells release this molecule into a tumour, where it turns arriving monocytes into cells that shut down the killers. organism: Mouse tissue_or_cell_type: B cell, monocyte and tumour experimental_model: Identification of a metabolite secreted by activated B cells, with monocyte differentiation and two genetic tests in mice limitations: The B cell-specific enzyme deletion is what makes the source assignment strong. The enzyme deleted is GAD67, not the GAD65 that is the diabetes autoantigen. exposure: B cell-derived GABA, with B cell deficiency and B cell-specific inactivation of the GABA-generating enzyme GAD67 evidence_span: {"source_cache": "artifacts/gaba-research/34732892.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b", "start_char": 0, "end_char": 878, "text_sha256": "907d2a95afcac30a55ebfa4a6056c31ca53c452caff350ded70a60c9fc2eb17b"} [gb-p34732892] B cell-derived GABA elicits IL-10+ macrophages to limit anti-tumour immunity. (2021). https://pubmed.ncbi.nlm.nih.gov/34732892/ DOI: 10.1038/s41586-021-04082-1
    Complete structured claim and evidence

  2. Production of IL4, IL6 and IL10 was unchanged during the reported zinc-deficiency experiment, unlike the TH1-associated cytokines.

    Zinc → T-cell IL4, IL6 and IL10 production profile source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Interleukin 4 (measured_cytokine); interleukin 6 (measured_cytokine); Interleukin 10 (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 did not suppress every cytokine in the same way.
    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 1392–1405

    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-th2-null Production of IL4, IL6 and IL10 was unchanged during the reported zinc-deficiency experiment, unlike the TH1-associated cytokines. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage did not suppress every cytokine in the same way. 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 4 (measured_cytokine); interleukin 6 (measured_cytokine); Interleukin 10 (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