Component

Human Toll-like receptor 2 / TLR2

Human Toll-like receptor 2 / TLR2. Species, exposure and limitations are retained in each linked claim.

6 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. Extracellular YARS1 activated TLR2 signaling and inflammatory mediator release in human monocyte/macrophage preparations.

    Human cytosolic tyrosyl-tRNA synthetase / YARS1 → Human Toll-like receptor 2 / TLR2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text and abstract
    experimental_model
    THP1 and peripheral-blood-derived macrophages; purified protein exposure.
    limitations
    This differs from intracellular charging and from assays of individual fragments.
    nutrient_topic
    L-Tyrosine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Tyrosine
    plain_language
    A protein used for translation also signals outside cells.
    primary_references
    Moonlighting matrix metalloproteinase substrates: Enhancement of proinflammatory functions of extracellular tyrosyl-tRNA synthetase upon cleavage. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31771979/ · DOI 10.1074/jbc.RA119.010486

    L-Tyrosine: catecholamines, thyroid chemistry, pigment, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 108–114

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · THP1 and peripheral-blood-derived macrophages; purified protein exposure. · source_derived_draft · unverified_draft

    ## l-tyrosine-yrs-tlr2 A protein used for translation also signals outside cells. Extracellular YARS1 activated TLR2 signaling and inflammatory mediator release in human monocyte/macrophage preparations. Model: THP1 and peripheral-blood-derived macrophages; purified protein exposure. Limitations: This differs from intracellular charging and from assays of individual fragments. Evidence access: Primary full text and abstract Moonlighting matrix metalloproteinase substrates: Enhancement of proinflammatory functions of extracellular tyrosyl-tRNA synthetase upon cleavage. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31771979/ · DOI 10.1074/jbc.RA119.010486
    Complete structured claim and evidence

  2. Low-DM pectin bound TLR2 with results consistent with electrostatic interaction of free galacturonate groups and positively charged receptor regions.

    Low-methylesterified lemon pectin, DM7 preparation → Human Toll-like receptor 2 / TLR2 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
    Exposed acidic groups can interact directly with an immune receptor.
    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 347–358

    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-tlr2-binding Low-DM pectin bound TLR2 with results consistent with electrostatic interaction of free galacturonate groups and positively charged receptor regions. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Exposed acidic groups can interact directly with an immune receptor. 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

Where it participates (unsigned role)

  1. Dectin-1 is recruited to phagosomes containing zymosan particles but not to phagosomes containing immunoglobulin G-opsonised particles, dectin-1 expression enhances Toll-like receptor-mediated activation of nuclear factor kappa B by beta-glucan-containing particles, and in macrophages and dendritic cells dectin-1 and Toll-like receptors are synergistic in mediating production of cytokines such as interleukin 12 and tumour necrosis factor alpha, while dectin-1 triggers production of reactive oxygen species, an inflammatory response that is primed by Toll-like receptor activation.

    Dectin-1 / CLEC7A → Activation of nuclear factor kappa B source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/12719479.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425", "start_char": 0, "end_char": 1588, "text_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425"}
    experimental_model
    Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement
    exposure
    Beta-glucan-containing zymosan particles on cells expressing dectin-1 with and without Toll-like receptor signalling
    limitations
    The particle is zymosan, which carries mannan and other yeast wall components as well as glucan, so a response to zymosan is not by itself a response to purified beta-glucan.
    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
    Mouse
    plain_language
    The glucan receptor does not work alone; paired with a bacterial sensor the same particle produces far more than either would.
    primary_references
    [bg-p12719479] Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. (2003). https://pubmed.ncbi.nlm.nih.gov/12719479/ DOI: 10.1084/jem.20021787
    tissue_or_cell_type
    Macrophage and 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 190–201

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement · source_derived_draft · unverified_draft

    ### bg-dectin1-works-with-tlr2 Dectin-1 is recruited to phagosomes containing zymosan particles but not to phagosomes containing immunoglobulin G-opsonised particles, dectin-1 expression enhances Toll-like receptor-mediated activation of nuclear factor kappa B by beta-glucan-containing particles, and in macrophages and dendritic cells dectin-1 and Toll-like receptors are synergistic in mediating production of cytokines such as interleukin 12 and tumour necrosis factor alpha, while dectin-1 triggers production of reactive oxygen species, an inflammatory response that is primed by Toll-like receptor activation. 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: The glucan receptor does not work alone; paired with a bacterial sensor the same particle produces far more than either would. organism: Mouse tissue_or_cell_type: Macrophage and dendritic cell experimental_model: Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement limitations: The particle is zymosan, which carries mannan and other yeast wall components as well as glucan, so a response to zymosan is not by itself a response to purified beta-glucan. exposure: Beta-glucan-containing zymosan particles on cells expressing dectin-1 with and without Toll-like receptor signalling evidence_span: {"source_cache": "artifacts/glucan-research/12719479.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425", "start_char": 0, "end_char": 1588, "text_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425"} [bg-p12719479] Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. (2003). https://pubmed.ncbi.nlm.nih.gov/12719479/ DOI: 10.1084/jem.20021787
    Complete structured claim and evidence

  2. Maximum plasma concentrations for glucan phosphate occurred at 4 hours while laminarin and scleroglucan showed two plasma peaks between 0.5 and 12 hours, at 24 hours 27 plus or minus 3% of the glucan phosphate and 20 plus or minus 7% of the laminarin remained in the serum, following oral administration glucans were bound and internalized by intestinal epithelial cells and gut-associated lymphoid tissue cells with internalization by intestinal epithelial cells not being Dectin-dependent, gut-associated lymphoid tissue expression of Dectin-1 and Toll-like receptor 2 but not Toll-like receptor 4 increased, oral glucan increased systemic levels of interleukin-12 by 151%, and oral glucan administration also increased survival in mice challenged with Staphylococcus aureus or Candida albicans.

    Glucan phosphate → Serum beta-glucan concentration after oral dosing source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/15976018.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18", "start_char": 0, "end_char": 1617, "text_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18"}
    experimental_model
    Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice
    exposure
    Glucan phosphate, laminarin and scleroglucan at 1 milligram per kilogram orally in rats, and 1 milligram orally in mice
    limitations
    Rodent pharmacokinetics and rodent challenge models. The reported figure for glucan phosphate at 24 hours is a percentage remaining in serum whose denominator the abstract does not state, so it is not read here as a fraction of the swallowed dose.
    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
    Rat and mouse
    plain_language
    In rodents the swallowed sugar does cross into the circulation, is taken up by the gut immune tissue, and leaves the animals better able to survive an infection.
    primary_references
    [bg-p15976018] Oral delivery and gastrointestinal absorption of soluble glucans stimulate increased resistance to infectious challenge. (2005). https://pubmed.ncbi.nlm.nih.gov/15976018/ DOI: 10.1124/jpet.105.085415
    tissue_or_cell_type
    Plasma, intestinal epithelium and gut-associated lymphoid tissue

    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 372–383

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice · source_derived_draft · unverified_draft

    ### bg-oral-glucan-does-reach-the-blood Maximum plasma concentrations for glucan phosphate occurred at 4 hours while laminarin and scleroglucan showed two plasma peaks between 0.5 and 12 hours, at 24 hours 27 plus or minus 3% of the glucan phosphate and 20 plus or minus 7% of the laminarin remained in the serum, following oral administration glucans were bound and internalized by intestinal epithelial cells and gut-associated lymphoid tissue cells with internalization by intestinal epithelial cells not being Dectin-dependent, gut-associated lymphoid tissue expression of Dectin-1 and Toll-like receptor 2 but not Toll-like receptor 4 increased, oral glucan increased systemic levels of interleukin-12 by 151%, and oral glucan administration also increased survival in mice challenged with Staphylococcus aureus or Candida albicans. 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: In rodents the swallowed sugar does cross into the circulation, is taken up by the gut immune tissue, and leaves the animals better able to survive an infection. organism: Rat and mouse tissue_or_cell_type: Plasma, intestinal epithelium and gut-associated lymphoid tissue experimental_model: Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice limitations: Rodent pharmacokinetics and rodent challenge models. The reported figure for glucan phosphate at 24 hours is a percentage remaining in serum whose denominator the abstract does not state, so it is not read here as a fraction of the swallowed dose. exposure: Glucan phosphate, laminarin and scleroglucan at 1 milligram per kilogram orally in rats, and 1 milligram orally in mice evidence_span: {"source_cache": "artifacts/glucan-research/15976018.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18", "start_char": 0, "end_char": 1617, "text_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18"} [bg-p15976018] Oral delivery and gastrointestinal absorption of soluble glucans stimulate increased resistance to infectious challenge. (2005). https://pubmed.ncbi.nlm.nih.gov/15976018/ DOI: 10.1124/jpet.105.085415
    Complete structured claim and evidence

  3. MMP cleavage of YARS1 increased TLR2 signaling, TNF secretion and chemotaxis relative to unprocessed YARS1.

    Human matrix metalloproteinase 8 / MMP8 → Human YARS1 proteolysis-dependent inflammatory signaling source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text and abstract
    experimental_model
    Protein cleavage and macrophage assays; MMP7 and MMP8 among tested enzymes.
    limitations
    A proposed feed-forward inflammatory loop still requires in vivo testing.
    nutrient_topic
    L-Tyrosine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Tyrosine
    plain_language
    Protease activity changes the strength of an extracellular signal.
    primary_references
    Moonlighting matrix metalloproteinase substrates: Enhancement of proinflammatory functions of extracellular tyrosyl-tRNA synthetase upon cleavage. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31771979/ · DOI 10.1074/jbc.RA119.010486

    L-Tyrosine: catecholamines, thyroid chemistry, pigment, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 116–122

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Protein cleavage and macrophage assays; MMP7 and MMP8 among tested enzymes. · source_derived_draft · unverified_draft

    ## l-tyrosine-yrs-proteolysis Protease activity changes the strength of an extracellular signal. MMP cleavage of YARS1 increased TLR2 signaling, TNF secretion and chemotaxis relative to unprocessed YARS1. Model: Protein cleavage and macrophage assays; MMP7 and MMP8 among tested enzymes. Limitations: A proposed feed-forward inflammatory loop still requires in vivo testing. Evidence access: Primary full text and abstract Moonlighting matrix metalloproteinase substrates: Enhancement of proinflammatory functions of extracellular tyrosyl-tRNA synthetase upon cleavage. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31771979/ · DOI 10.1074/jbc.RA119.010486
    Complete structured claim and evidence

  4. DM7 binding was lower to R315Q/R316Q/R321Q/K347Q TLR2 than to the R321Q/K347Q construct.

    Human TLR2 R315Q/R316Q/R321Q/K347Q construct → Low-methylesterified lemon pectin, DM7 preparation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/pectin-research/29545800.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4b9e856ec2420c457b98f455ec243b742525b63d9382b69ef087456e0136cb42", "start_char": 37198, "end_char": 38286, "text_sha256": "1e7101498d68b59ef3b4b7d5ad57ce9d4aa25f535bc5000e421099adc8720b19"}
    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
    Changing the receptor charges weakens the measured interaction.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 412–423

    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-tlr2-mutant DM7 binding was lower to R315Q/R316Q/R321Q/K347Q TLR2 than to the R321Q/K347Q construct. Condition category: machinery_impairment nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the receptor charges weakens the measured interaction. 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.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4b9e856ec2420c457b98f455ec243b742525b63d9382b69ef087456e0136cb42", "start_char": 37198, "end_char": 38286, "text_sha256": "1e7101498d68b59ef3b4b7d5ad57ce9d4aa25f535bc5000e421099adc8720b19"} [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.

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