Component

Interleukin-23

Heterodimeric inflammatory cytokine, distinct from IL-12p70.

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 acts on it

  1. RA with IL-15 promoted dendritic-cell IL-23 release.

    All-trans-retinoic acid → Interleukin-23 source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract and Figure 3
    experimental_model
    Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models.
    exposure
    RA plus IL-15
    limitations
    Different context from isolated naive T-cell induction.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    RA participates in a proinflammatory response in this cytokine setting.
    primary_references
    [va-depaolo-2011] Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens (2011). https://www.nature.com/articles/nature09849 DOI: 10.1038/nature09849
    tissue_or_cell_type
    Dendritic cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1305–1316

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models. · source_derived_draft · unverified_draft

    ### va-sig-ra-il15-il23 RA with IL-15 promoted dendritic-cell IL-23 release. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA participates in a proinflammatory response in this cytokine setting. organism: Mus musculus tissue_or_cell_type: Dendritic cells experimental_model: Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models. limitations: Different context from isolated naive T-cell induction. evidence_locator: Abstract and Figure 3 exposure: RA plus IL-15 [va-depaolo-2011] Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens (2011). https://www.nature.com/articles/nature09849 DOI: 10.1038/nature09849
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu.

    Particle size of a glucan preparation → Interleukin-1 beta / IL1B source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"}
    experimental_model
    Comparison of large and small beta-glucan particles on human dendritic cell cytokine output
    exposure
    Large against small particulate beta-glucans, with assessment of phagocytosis
    limitations
    Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Human
    plain_language
    Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all.
    primary_references
    [bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791
    tissue_or_cell_type
    Monocyte-derived dendritic cell

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 177–188

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of large and small beta-glucan particles on human dendritic cell cytokine output · source_derived_draft · unverified_draft

    ### bg-particle-size-sets-the-cytokines Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all. organism: Human tissue_or_cell_type: Monocyte-derived dendritic cell experimental_model: Comparison of large and small beta-glucan particles on human dendritic cell cytokine output limitations: Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that. exposure: Large against small particulate beta-glucans, with assessment of phagocytosis evidence_span: {"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"} [bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791
    Complete structured claim and evidence

  2. Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program.

    Sodium chloride → Mouse IL-23 receptor expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
    experimental_model
    T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
    exposure
    NaCl elevation and Sgk1 perturbation
    limitations
    The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    Salt exposure can reinforce responsiveness to an immune signal in this model.
    primary_references
    [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    tissue_or_cell_type
    IL-23-responsive TH17 cells

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 577–588

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft

    ### sodium-salt-il23r Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Salt exposure can reinforce responsiveness to an immune signal in this model. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    Complete structured claim and evidence

  3. The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program.

    Serum and glucocorticoid-regulated kinase 1 → Mouse forkhead transcription factor Foxo1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
    experimental_model
    T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
    exposure
    NaCl elevation and Sgk1 perturbation
    limitations
    The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    The same kinase family used in kidney salt handling has another role in immune cells.
    primary_references
    [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    tissue_or_cell_type
    IL-23-responsive TH17 cells

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 551–562

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft

    ### sodium-sgk-foxo The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same kinase family used in kidney salt handling has another role in immune cells. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    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.

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