Component

T cell

The primary cellular context of the featured pathway.

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

Where it participates (unsigned role)

  1. There were 5, 8 and 13 different GABA-A subunit isoforms identified in human, mouse and rat CD4-positive and CD8-positive T cells respectively, importantly the gamma2 subunit that imposes benzodiazepine sensitivity on the GABA-A receptors was only detected in the mouse T cells, immunoblots and immunocytochemistry showed abundant GABA-A channel proteins in T cells from all three species, GABA-activated whole-cell transient and tonic currents were recorded and were inhibited by picrotoxin, SR95531 and bicuculline, and it is important to bear in mind the interspecies difference when selecting the appropriate animal models and when selecting drugs aimed at modulating human T cell function.

    The GABA-A receptor subunit repertoire of a cell → GABA-A receptor anion channels source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/22927941.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0457001832d2a3595899415221b7797f5288a787c1d52fd6afa1acf24f032402", "start_char": 0, "end_char": 1589, "text_sha256": "0457001832d2a3595899415221b7797f5288a787c1d52fd6afa1acf24f032402"}
    experimental_model
    Subunit isoform survey with immunoblotting, immunocytochemistry and whole-cell recording across three species
    exposure
    GABA-activated transient and tonic currents, with picrotoxin, SR95531 and bicuculline
    limitations
    The species comparison is the point. Subunit repertoires differ enough that a drug result in one species does not carry to another.
    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
    Human, mouse and rat
    plain_language
    The subunit that makes a receptor respond to benzodiazepines was found on mouse T cells and not on human ones.
    primary_references
    [gb-p22927941] Different subtypes of GABA-A receptors are expressed in human, mouse and rat T lymphocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22927941/ DOI: 10.1371/journal.pone.0042959
    tissue_or_cell_type
    CD4 and CD8 T lymphocytes

    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 521–532

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Subunit isoform survey with immunoblotting, immunocytochemistry and whole-cell recording across three species · source_derived_draft · unverified_draft

    ### gb-the-subunits-differ-by-species There were 5, 8 and 13 different GABA-A subunit isoforms identified in human, mouse and rat CD4-positive and CD8-positive T cells respectively, importantly the gamma2 subunit that imposes benzodiazepine sensitivity on the GABA-A receptors was only detected in the mouse T cells, immunoblots and immunocytochemistry showed abundant GABA-A channel proteins in T cells from all three species, GABA-activated whole-cell transient and tonic currents were recorded and were inhibited by picrotoxin, SR95531 and bicuculline, and it is important to bear in mind the interspecies difference when selecting the appropriate animal models and when selecting drugs aimed at modulating human T cell function. 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: The subunit that makes a receptor respond to benzodiazepines was found on mouse T cells and not on human ones. organism: Human, mouse and rat tissue_or_cell_type: CD4 and CD8 T lymphocytes experimental_model: Subunit isoform survey with immunoblotting, immunocytochemistry and whole-cell recording across three species limitations: The species comparison is the point. Subunit repertoires differ enough that a drug result in one species does not carry to another. exposure: GABA-activated transient and tonic currents, with picrotoxin, SR95531 and bicuculline evidence_span: {"source_cache": "artifacts/gaba-research/22927941.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0457001832d2a3595899415221b7797f5288a787c1d52fd6afa1acf24f032402", "start_char": 0, "end_char": 1589, "text_sha256": "0457001832d2a3595899415221b7797f5288a787c1d52fd6afa1acf24f032402"} [gb-p22927941] Different subtypes of GABA-A receptors are expressed in human, mouse and rat T lymphocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22927941/ DOI: 10.1371/journal.pone.0042959
    Complete structured claim and evidence

  2. RA during mouse T-cell activation increased CCR9 expression.

    All-trans-retinoic acid → C-C chemokine receptor 9 source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice.
    exposure
    Added RA
    limitations
    Receptor expression is distinct from clinical infection protection.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Activated cells acquire a receptor associated with gut entry.
    primary_references
    [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    tissue_or_cell_type
    Activated T cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1175–1186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-ra-ccr9 RA during mouse T-cell activation increased CCR9 expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activated cells acquire a receptor associated with gut entry. organism: Mus musculus tissue_or_cell_type: Activated T cells experimental_model: Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. limitations: Receptor expression is distinct from clinical infection protection. evidence_locator: Abstract exposure: Added RA [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    Complete structured claim and evidence

  3. 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

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