Component

T-cell proliferation, model specified

Study-scoped entity; inspect species, exposure and experimental limitations 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.

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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. We examined in encephalitogenic T cells if they expressed functional GABA channels that could be activated by the low nanomolar to 1 micromolar physiological concentrations of GABA present around neurons in the brain, the cells expressed the alpha1, alpha4, beta2, beta3, gamma1 and delta GABA-A channel subunits and formed functional extrasynaptic-like GABA channels that were activated by 1 micromolar GABA, and 100 nanomolar and higher GABA concentrations decreased T cell proliferation.

    Gamma-aminobutyric acid → T-cell proliferation, model specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/18954912.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3723b5b4b643817af252230d67dafbc0b5ca2deadb17cdbdbc9f340ddfc6a472", "start_char": 0, "end_char": 728, "text_sha256": "3723b5b4b643817af252230d67dafbc0b5ca2deadb17cdbdbc9f340ddfc6a472"}
    experimental_model
    Patch clamp and proliferation assays on encephalitogenic T cells at physiological GABA concentrations
    exposure
    GABA at nanomolar to micromolar concentrations, the range present around neurons
    limitations
    A small subunit and function study in one T cell type. It measures the concentration range that matters rather than assuming it.
    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
    Rat
    plain_language
    These cells carry the kind of channel built for a steady background level rather than a synaptic pulse, and that background level slows them down.
    primary_references
    [gb-p18954912] GABA, a natural immunomodulator of T lymphocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18954912/ DOI: 10.1016/j.jneuroim.2008.08.017
    tissue_or_cell_type
    Encephalitogenic T cell

    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 508–519

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patch clamp and proliferation assays on encephalitogenic T cells at physiological GABA concentrations · source_derived_draft · unverified_draft

    ### gb-t-cells-read-ambient-gaba We examined in encephalitogenic T cells if they expressed functional GABA channels that could be activated by the low nanomolar to 1 micromolar physiological concentrations of GABA present around neurons in the brain, the cells expressed the alpha1, alpha4, beta2, beta3, gamma1 and delta GABA-A channel subunits and formed functional extrasynaptic-like GABA channels that were activated by 1 micromolar GABA, and 100 nanomolar and higher GABA concentrations decreased T cell proliferation. 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: These cells carry the kind of channel built for a steady background level rather than a synaptic pulse, and that background level slows them down. organism: Rat tissue_or_cell_type: Encephalitogenic T cell experimental_model: Patch clamp and proliferation assays on encephalitogenic T cells at physiological GABA concentrations limitations: A small subunit and function study in one T cell type. It measures the concentration range that matters rather than assuming it. exposure: GABA at nanomolar to micromolar concentrations, the range present around neurons evidence_span: {"source_cache": "artifacts/gaba-research/18954912.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3723b5b4b643817af252230d67dafbc0b5ca2deadb17cdbdbc9f340ddfc6a472", "start_char": 0, "end_char": 728, "text_sha256": "3723b5b4b643817af252230d67dafbc0b5ca2deadb17cdbdbc9f340ddfc6a472"} [gb-p18954912] GABA, a natural immunomodulator of T lymphocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18954912/ DOI: 10.1016/j.jneuroim.2008.08.017
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A subset of GABA-A receptor subunits are expressed by CD4-positive T cells including the delta subunit that confers high affinity for GABA and sensitivity to alcohol, GABA at relatively low concentrations down-regulated effector T cell responses to beta cell antigens ex vivo and administration of GABA retarded the adoptive transfer of type 1 diabetes in NOD/scid mice, treatment with a low dose of GABA at 600 micrograms daily dramatically inhibited the development of proinflammatory T cell responses and disease progression in disease-prone mice that already had established autoimmunity, and GABA inhibited T cell receptor-mediated T cell cycle progression in vitro which may underlie the therapeutic effects.

    Gamma-aminobutyric acid → Type 1 diabetes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/15470076.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09", "start_char": 0, "end_char": 1443, "text_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09"}
    experimental_model
    Subunit analysis with ex vivo antigen responses, adoptive transfer and treatment of disease-prone mice
    exposure
    GABA at low concentrations ex vivo, and 600 micrograms daily in mice with established autoimmunity
    limitations
    A mouse type 1 diabetes model. The cell cycle result offers a mechanism for the disease effect but is measured separately from it.
    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
    Low doses slowed the immune attack on the insulin-producing cells even after that attack had already started.
    primary_references
    [gb-p15470076] Gamma-aminobutyric acid inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model. (2004). https://pubmed.ncbi.nlm.nih.gov/15470076/ DOI: 10.4049/jimmunol.173.8.5298
    tissue_or_cell_type
    CD4 T cell and pancreatic islet

    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 534–545

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Subunit analysis with ex vivo antigen responses, adoptive transfer and treatment of disease-prone mice · source_derived_draft · unverified_draft

    ### gb-gaba-slows-the-autoimmune-t-cell A subset of GABA-A receptor subunits are expressed by CD4-positive T cells including the delta subunit that confers high affinity for GABA and sensitivity to alcohol, GABA at relatively low concentrations down-regulated effector T cell responses to beta cell antigens ex vivo and administration of GABA retarded the adoptive transfer of type 1 diabetes in NOD/scid mice, treatment with a low dose of GABA at 600 micrograms daily dramatically inhibited the development of proinflammatory T cell responses and disease progression in disease-prone mice that already had established autoimmunity, and GABA inhibited T cell receptor-mediated T cell cycle progression in vitro which may underlie the therapeutic effects. 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: Low doses slowed the immune attack on the insulin-producing cells even after that attack had already started. organism: Mouse tissue_or_cell_type: CD4 T cell and pancreatic islet experimental_model: Subunit analysis with ex vivo antigen responses, adoptive transfer and treatment of disease-prone mice limitations: A mouse type 1 diabetes model. The cell cycle result offers a mechanism for the disease effect but is measured separately from it. exposure: GABA at low concentrations ex vivo, and 600 micrograms daily in mice with established autoimmunity evidence_span: {"source_cache": "artifacts/gaba-research/15470076.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09", "start_char": 0, "end_char": 1443, "text_sha256": "e5523c02fc4571d5ab6c23776794b4b5cf025fb86cdba9acdc12011f3a6b2e09"} [gb-p15470076] Gamma-aminobutyric acid inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model. (2004). https://pubmed.ncbi.nlm.nih.gov/15470076/ DOI: 10.4049/jimmunol.173.8.5298
    Complete structured claim and evidence

  2. Arginine removal lowered CD3-zeta and proliferation; replacing arginine reversed the changes.

    Experimental arginine-depleted culture medium → Human T-cell receptor CD3-zeta chain / CD247 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Jurkat T cells in arginine-free culture medium.
    limitations
    Not a clinical dietary-deficiency threshold.
    nutrient_topic
    L-Arginine collection; tissue, species, dose and formulation distinctions retained. · L-Arginine
    plain_language
    The receptor’s signaling machinery could recover when arginine returned.
    primary_references
    Regulation of T cell receptor CD3zeta chain expression by L-arginine. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11950832/ · DOI 10.1074/jbc.m110675200
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Arginine: transport, metabolic branches, nutrient interactions, availability and discovery questions (2026-09-18) · lines 278–284

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Jurkat T cells in arginine-free culture medium. · source_derived_draft · unverified_draft

    ## arg-jurkat-protein The receptor’s signaling machinery could recover when arginine returned. Arginine removal lowered CD3-zeta and proliferation; replacing arginine reversed the changes. Model: Jurkat T cells in arginine-free culture medium. Limitations: Not a clinical dietary-deficiency threshold. Evidence access: Primary abstract Regulation of T cell receptor CD3zeta chain expression by L-arginine. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11950832/ · DOI 10.1074/jbc.m110675200
    Complete structured claim and evidence

In the sources

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