Component

TLR2-TLR1 receptor complex

Study-defined TLR2-TLR1 receptor complex. Read each linked record for species, exposure and endpoint.

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. TLR activation increased vitamin D1-alpha-hydroxylase gene expression in human macrophages.

    TLR2-TLR1 receptor complex → CYP27B1 mRNA source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay
    exposure
    TLR activation in cultured human monocytes/macrophages.
    limitations
    Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    A pathogen-sensing signal increased part of the local vitamin D machinery.
    primary_references
    [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933
    tissue_or_cell_type
    Human monocytes/macrophages

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 957–968

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay · source_derived_draft · unverified_draft

    ### vd-tlr-cyp27b1 TLR activation increased vitamin D1-alpha-hydroxylase gene expression in human macrophages. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pathogen-sensing signal increased part of the local vitamin D machinery. organism: Homo sapiens tissue_or_cell_type: Human monocytes/macrophages experimental_model: Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay limitations: Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling. exposure: TLR activation in cultured human monocytes/macrophages. cross_nutrient: false [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933
    Complete structured claim and evidence

  2. TLR activation coupled vitamin D pathway induction to cathelicidin expression and killing of intracellular M. tuberculosis in the human macrophage experiments.

    TLR2-TLR1 receptor complex → Intracellular Mycobacterium tuberculosis viability source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay
    exposure
    Cultured human macrophages with intracellular M. tuberculosis.
    limitations
    Cellular experimental result, not a human tuberculosis-treatment trial; infection response depends on more than vitamin D.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    The cell experiment linked local vitamin D signaling to bacterial killing.
    primary_references
    [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933
    tissue_or_cell_type
    Human macrophages

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 970–981

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay · source_derived_draft · unverified_draft

    ### vd-tlr-mycobacteria TLR activation coupled vitamin D pathway induction to cathelicidin expression and killing of intracellular M. tuberculosis in the human macrophage experiments. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell experiment linked local vitamin D signaling to bacterial killing. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay limitations: Cellular experimental result, not a human tuberculosis-treatment trial; infection response depends on more than vitamin D. exposure: Cultured human macrophages with intracellular M. tuberculosis. cross_nutrient: false [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933
    Complete structured claim and evidence

  3. TLR activation increased VDR gene expression in human macrophages.

    TLR2-TLR1 receptor complex → Human VDR mRNA source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay
    exposure
    TLR activation in cultured human monocytes/macrophages.
    limitations
    Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    A pathogen-sensing signal increased part of the local vitamin D machinery.
    primary_references
    [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933
    tissue_or_cell_type
    Human monocytes/macrophages

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 944–955

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay · source_derived_draft · unverified_draft

    ### vd-tlr-vdr TLR activation increased VDR gene expression in human macrophages. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pathogen-sensing signal increased part of the local vitamin D machinery. organism: Homo sapiens tissue_or_cell_type: Human monocytes/macrophages experimental_model: Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay limitations: Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling. exposure: TLR activation in cultured human monocytes/macrophages. cross_nutrient: false [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933
    Complete structured claim and evidence

What acts on it

  1. Low-DM pectin inhibited stimulated TLR2-TLR1 signaling in the tested assays.

    Low-methylesterified lemon pectin, DM7 preparation → TLR2-TLR1 receptor complex source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/pectin-research/29545800.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c194f301d46822febd69d3bc9768bd31de73e5dd2ca87f0d3b0e64cd4726dc65", "start_char": 0, "end_char": 1540, "text_sha256": "c194f301d46822febd69d3bc9768bd31de73e5dd2ca87f0d3b0e64cd4726dc65"}
    experimental_model
    Receptor binding, reporter cells, human dendritic cells and mouse ileitis model
    exposure
    Lemon pectin DM7 versus DM75; cell exposures 1-100 micrograms/mL; mice 3 mg/day before doxorubicin
    limitations
    Model-specific. Binding and cytokine experiments do not establish prevention of human inflammatory disease. Lack of increased measured SCFAs does not exclude every microbial contribution.
    nutrient_topic
    Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides
    organism
    Human receptor/cell assays; Mus musculus separately scoped
    plain_language
    This pectin preparation reduced one receptor-pair signal.
    primary_references
    [pectin-p29545800] Dietary Fiber Pectin Directly Blocks Toll-Like Receptor 2-1 and Prevents Doxorubicin-Induced Ileitis. (2018). https://pubmed.ncbi.nlm.nih.gov/29545800/ DOI: 10.3389/fimmu.2018.00383
    tissue_or_cell_type
    Innate immune receptors and intestine

    Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 360–371

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor binding, reporter cells, human dendritic cells and mouse ileitis model · source_derived_draft · unverified_draft

    ### pectin-tlr21-inhibition Low-DM pectin inhibited stimulated TLR2-TLR1 signaling in the tested assays. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This pectin preparation reduced one receptor-pair signal. organism: Human receptor/cell assays; Mus musculus separately scoped tissue_or_cell_type: Innate immune receptors and intestine experimental_model: Receptor binding, reporter cells, human dendritic cells and mouse ileitis model limitations: Model-specific. Binding and cytokine experiments do not establish prevention of human inflammatory disease. Lack of increased measured SCFAs does not exclude every microbial contribution. exposure: Lemon pectin DM7 versus DM75; cell exposures 1-100 micrograms/mL; mice 3 mg/day before doxorubicin evidence_span: {"source_cache": "artifacts/pectin-research/29545800.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c194f301d46822febd69d3bc9768bd31de73e5dd2ca87f0d3b0e64cd4726dc65", "start_char": 0, "end_char": 1540, "text_sha256": "c194f301d46822febd69d3bc9768bd31de73e5dd2ca87f0d3b0e64cd4726dc65"} [pectin-p29545800] Dietary Fiber Pectin Directly Blocks Toll-Like Receptor 2-1 and Prevents Doxorubicin-Induced Ileitis. (2018). https://pubmed.ncbi.nlm.nih.gov/29545800/ DOI: 10.3389/fimmu.2018.00383
    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