Component

Beta-glucan

Beta-glucan. A family of glucose polymers defined by their linkage pattern rather than a single compound; the preparations in this collection differ in backbone, branching, molecular weight, conformation, solubility, particle size and purity, and each is recorded as its own entity with no family link joining them, because those differences determine which receptor engages and whether engagement signals at all. Species, exposure and limitations are retained in each linked claim.

7 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. In a randomised open-label intervention pilot study in 15 healthy male volunteers, subjects in the beta-glucan group ingested beta-glucan 1000 milligrams once daily for 7 days, beta-glucan was barely detectable in serum of volunteers at all time-points, and neither cytokine production nor microbicidal activity of leukocytes were affected by orally administered beta-glucan, so the present study does not support the use of oral beta-glucan to enhance innate immune responses in humans.

    Beta-glucan → Ex vivo cytokine production by stimulated leukocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/25268806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b", "start_char": 0, "end_char": 1307, "text_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b"}
    experimental_model
    Randomised open-label intervention pilot study in 15 healthy male volunteers
    exposure
    Oral beta-glucan 1000 milligrams once daily for 7 days against no treatment, with serial sampling
    limitations
    Ten treated and five control subjects, one product, one dose, seven days, and ex vivo readouts. A negative pilot of this size does not establish that all oral preparations are inactive.
    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
    Ten healthy men took a gram a day for a week; almost none of it showed up in the blood and nothing measurable changed.
    primary_references
    [bg-p25268806] The effects of orally administered Beta-glucan on innate immune responses in humans, a randomized open-label intervention pilot-study. (2014). https://pubmed.ncbi.nlm.nih.gov/25268806/ DOI: 10.1371/journal.pone.0108794
    tissue_or_cell_type
    Serum and peripheral leukocytes

    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 385–396

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised open-label intervention pilot study in 15 healthy male volunteers · source_derived_draft · unverified_draft

    ### bg-in-people-nothing-was-detectable In a randomised open-label intervention pilot study in 15 healthy male volunteers, subjects in the beta-glucan group ingested beta-glucan 1000 milligrams once daily for 7 days, beta-glucan was barely detectable in serum of volunteers at all time-points, and neither cytokine production nor microbicidal activity of leukocytes were affected by orally administered beta-glucan, so the present study does not support the use of oral beta-glucan to enhance innate immune responses in humans. 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: Ten healthy men took a gram a day for a week; almost none of it showed up in the blood and nothing measurable changed. organism: Human tissue_or_cell_type: Serum and peripheral leukocytes experimental_model: Randomised open-label intervention pilot study in 15 healthy male volunteers limitations: Ten treated and five control subjects, one product, one dose, seven days, and ex vivo readouts. A negative pilot of this size does not establish that all oral preparations are inactive. exposure: Oral beta-glucan 1000 milligrams once daily for 7 days against no treatment, with serial sampling evidence_span: {"source_cache": "artifacts/glucan-research/25268806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b", "start_char": 0, "end_char": 1307, "text_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b"} [bg-p25268806] The effects of orally administered Beta-glucan on innate immune responses in humans, a randomized open-label intervention pilot-study. (2014). https://pubmed.ncbi.nlm.nih.gov/25268806/ DOI: 10.1371/journal.pone.0108794
    Complete structured claim and evidence

  2. In comparison with antitumour monoclonal antibody or beta-glucan alone, combined treatment produced significantly greater tumour regression in all five models, tumour-free survival only occurred in models that incorporated stable expression of the target antigen, beta-glucan enhancement of the monoclonal antibody tumoricidal response did not occur in mice deficient in either leukocyte CR3 or serum C3 confirming the requirement for CR3 on leukocytes and iC3b on tumours, and granulocytes appeared to be primarily responsible for tumoricidal activity because beta-glucan therapeutic responses did not occur in granulocyte-depleted mice.

    Beta-glucan → Complement-activating antitumour monoclonal antibodies source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/glucan-research/14695221.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5", "start_char": 0, "end_char": 1827, "text_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5"}
    experimental_model
    Five mouse tumour models with antitumour monoclonal antibody, in CR3-deficient, C3-deficient and granulocyte-depleted animals
    exposure
    Intravenous beta-glucan combined with antitumour monoclonal antibodies in BALB/c and C57Bl/6 mice
    limitations
    Five models with genetic and depletion controls, which is what makes the requirement claim strong. Tumour-free survival occurred only where the target antigen was stably expressed.
    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
    Take away the complement protein, the receptor, or the granulocytes, and the effect disappears entirely.
    primary_references
    [bg-p14695221] Beta-glucan functions as an adjuvant for monoclonal antibody immunotherapy by recruiting tumoricidal granulocytes as killer cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14695221/
    tissue_or_cell_type
    Mammary, subcutaneous and hepatic tumours
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    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 229–240

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five mouse tumour models with antitumour monoclonal antibody, in CR3-deficient, C3-deficient and granulocyte-depleted animals · source_derived_draft · unverified_draft

    ### bg-needs-cr3-c3-and-granulocytes In comparison with antitumour monoclonal antibody or beta-glucan alone, combined treatment produced significantly greater tumour regression in all five models, tumour-free survival only occurred in models that incorporated stable expression of the target antigen, beta-glucan enhancement of the monoclonal antibody tumoricidal response did not occur in mice deficient in either leukocyte CR3 or serum C3 confirming the requirement for CR3 on leukocytes and iC3b on tumours, and granulocytes appeared to be primarily responsible for tumoricidal activity because beta-glucan therapeutic responses did not occur in granulocyte-depleted mice. Condition category: machinery_impairment 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: Take away the complement protein, the receptor, or the granulocytes, and the effect disappears entirely. organism: Mouse tissue_or_cell_type: Mammary, subcutaneous and hepatic tumours experimental_model: Five mouse tumour models with antitumour monoclonal antibody, in CR3-deficient, C3-deficient and granulocyte-depleted animals limitations: Five models with genetic and depletion controls, which is what makes the requirement claim strong. Tumour-free survival occurred only where the target antigen was stably expressed. exposure: Intravenous beta-glucan combined with antitumour monoclonal antibodies in BALB/c and C57Bl/6 mice evidence_span: {"source_cache": "artifacts/glucan-research/14695221.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5", "start_char": 0, "end_char": 1827, "text_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5"} [bg-p14695221] Beta-glucan functions as an adjuvant for monoclonal antibody immunotherapy by recruiting tumoricidal granulocytes as killer cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14695221/
    Complete structured claim and evidence

  3. When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state.

    Beta-glucan → The primed state of complement receptor 3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"}
    experimental_model
    Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets
    exposure
    Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar
    limitations
    An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient.
    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
    The sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill.
    primary_references
    [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777
    tissue_or_cell_type
    Neutrophil and natural killer 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 216–227

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets · source_derived_draft · unverified_draft

    ### bg-soluble-glucan-primes-cr3 When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state. 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 sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill. organism: Human tissue_or_cell_type: Neutrophil and natural killer cell experimental_model: Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets limitations: An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient. exposure: Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar evidence_span: {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"} [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777
    Complete structured claim and evidence

  4. Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice.

    Beta-glucan → Expansion of myeloid-lineage progenitors in the bone marrow source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"}
    experimental_model
    Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models
    exposure
    Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy
    limitations
    A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow.
    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 change is not only in the cells circulating now; it reaches the factory that makes the next ones.
    primary_references
    [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
    tissue_or_cell_type
    Bone marrow

    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 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models · source_derived_draft · unverified_draft

    ### bg-training-reaches-the-marrow Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice. 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 change is not only in the cells circulating now; it reaches the factory that makes the next ones. organism: Mouse tissue_or_cell_type: Bone marrow experimental_model: Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models limitations: A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow. exposure: Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy evidence_span: {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"} [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
    Complete structured claim and evidence

  5. Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms.

    Beta-glucan → Trained immunity, an altered response to a later challenge after the first has ended source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"}
    experimental_model
    Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo
    exposure
    Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge
    limitations
    The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route.
    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
    Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired.
    primary_references
    [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006
    tissue_or_cell_type
    Monocyte

    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 424–435

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo · source_derived_draft · unverified_draft

    ### bg-training-runs-through-raf1 Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms. 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: Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired. organism: Mouse tissue_or_cell_type: Monocyte experimental_model: Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo limitations: The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route. exposure: Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge evidence_span: {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"} [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006
    Complete structured claim and evidence

What acts on it

  1. CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated.

    The lectin site of CD11b C-terminal to the I-domain → Beta-glucan source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"}
    experimental_model
    Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies
    exposure
    Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide
    limitations
    Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone.
    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
    The complement receptor grips sugars at a second site, separate from the one that grips the complement fragment.
    primary_references
    [bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
    tissue_or_cell_type
    Leukocytes

    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 203–214

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies · source_derived_draft · unverified_draft

    ### bg-cr3-has-a-lectin-site CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated. 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 complement receptor grips sugars at a second site, separate from the one that grips the complement fragment. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies limitations: Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone. exposure: Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide evidence_span: {"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"} [bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
    Complete structured claim and evidence

  2. The carbohydrate polymers known as beta-1,3-D-glucans exert potent effects on the immune system, stimulating antitumour and antimicrobial activity for example, by binding to receptors on macrophages and other white blood cells and activating them, and although beta-glucans are known to bind to receptors such as complement receptor 3 there is evidence that another beta-glucan receptor is present on macrophages, which is identified here as dectin-1.

    Dectin-1 / CLEC7A → Beta-glucan source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/11544516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c", "start_char": 0, "end_char": 573, "text_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c"}
    experimental_model
    Identification of the unknown macrophage beta-glucan receptor
    exposure
    Beta-1,3-D-glucans binding to macrophage surface receptors
    limitations
    A brief communication announcing the identification. It states that beta-glucans were already known to bind complement receptor 3, so it adds a receptor rather than replacing one.
    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 and human cells
    plain_language
    A second receptor for these sugars was identified, alongside the complement receptor already known to bind them.
    primary_references
    [bg-p11544516] Immune recognition. A new receptor for beta-glucans. (2001). https://pubmed.ncbi.nlm.nih.gov/11544516/ DOI: 10.1038/35092620
    tissue_or_cell_type
    Macrophage

    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 99–110

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Identification of the unknown macrophage beta-glucan receptor · source_derived_draft · unverified_draft

    ### bg-dectin1-is-the-unknown-receptor The carbohydrate polymers known as beta-1,3-D-glucans exert potent effects on the immune system, stimulating antitumour and antimicrobial activity for example, by binding to receptors on macrophages and other white blood cells and activating them, and although beta-glucans are known to bind to receptors such as complement receptor 3 there is evidence that another beta-glucan receptor is present on macrophages, which is identified here as dectin-1. 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: A second receptor for these sugars was identified, alongside the complement receptor already known to bind them. organism: Mouse and human cells tissue_or_cell_type: Macrophage experimental_model: Identification of the unknown macrophage beta-glucan receptor limitations: A brief communication announcing the identification. It states that beta-glucans were already known to bind complement receptor 3, so it adds a receptor rather than replacing one. exposure: Beta-1,3-D-glucans binding to macrophage surface receptors evidence_span: {"source_cache": "artifacts/glucan-research/11544516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c", "start_char": 0, "end_char": 573, "text_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c"} [bg-p11544516] Immune recognition. A new receptor for beta-glucans. (2001). https://pubmed.ncbi.nlm.nih.gov/11544516/ DOI: 10.1038/35092620
    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