Dectin-1 / CLEC7A

evidence_span

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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

evidence_span

{"source_cache": "artifacts/glucan-research/12163569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "533d8630c3d727db58869724825f47c5241cf9c3159acce359d3bc8b0fdb2a6a", "start_char": 0, "end_char": 1365, "text_sha256": "533d8630c3d727db58869724825f47c5241cf9c3159acce359d3bc8b0fdb2a6a"}

experimental_model

Carbohydrate inhibition, CD11b-deficient cells and a new anti-Dectin-1 monoclonal antibody applied to non-opsonic zymosan binding

exposure

Zymosan binding to primary macrophages with specific carbohydrate inhibitors, CD11b deficiency, a blocking anti-CR3 antibody and the novel anti-Dectin-1 antibody 2A11

limitations

The ligand is zymosan, which is a mannan-rich particle as well as a glucan one, and the readout is non-opsonic binding rather than every glucan response.

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

Removing the complement receptor entirely did not change how macrophages grabbed yeast particles; blocking the other receptor did.

primary_references

[bg-p12163569] Dectin-1 is a major beta-glucan receptor on macrophages. (2002). https://pubmed.ncbi.nlm.nih.gov/12163569/ DOI: 10.1084/jem.20020470

tissue_or_cell_type

Primary 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 112–123

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carbohydrate inhibition, CD11b-deficient cells and a new anti-Dectin-1 monoclonal antibody applied to non-opsonic zymosan binding · source_derived_draft · unverified_draft

### bg-dectin1-not-cr3-binds-zymosan Non-opsonic zymosan binding was unaffected by genetic CD11b deficiency or a blocking monoclonal antibody against CR3, demonstrating that CR3 was not the beta-glucan receptor mediating this activity, and using the novel anti-Dectin-1 antibody 2A11 Dectin-1 was shown to be almost exclusively responsible for the beta-glucan-dependent non-opsonic recognition of zymosan by primary macrophages, defining Dectin-1 as the leukocyte beta-glucan receptor first described over 50 years ago and resolving the long-standing controversy regarding the identity of this important molecule. 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: Removing the complement receptor entirely did not change how macrophages grabbed yeast particles; blocking the other receptor did. organism: Mouse tissue_or_cell_type: Primary macrophage experimental_model: Carbohydrate inhibition, CD11b-deficient cells and a new anti-Dectin-1 monoclonal antibody applied to non-opsonic zymosan binding limitations: The ligand is zymosan, which is a mannan-rich particle as well as a glucan one, and the readout is non-opsonic binding rather than every glucan response. exposure: Zymosan binding to primary macrophages with specific carbohydrate inhibitors, CD11b deficiency, a blocking anti-CR3 antibody and the novel anti-Dectin-1 antibody 2A11 evidence_span: {"source_cache": "artifacts/glucan-research/12163569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "533d8630c3d727db58869724825f47c5241cf9c3159acce359d3bc8b0fdb2a6a", "start_char": 0, "end_char": 1365, "text_sha256": "533d8630c3d727db58869724825f47c5241cf9c3159acce359d3bc8b0fdb2a6a"} [bg-p12163569] Dectin-1 is a major beta-glucan receptor on macrophages. (2002). https://pubmed.ncbi.nlm.nih.gov/12163569/ DOI: 10.1084/jem.20020470

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

evidence_span

{"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"}

experimental_model

Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes

exposure

Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan

limitations

A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line.

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

Recombinant protein and a macrophage cell line

plain_language

The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire.

primary_references

[bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200

tissue_or_cell_type

Cell-free microarray and cultured cells

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 125–136

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes · source_derived_draft · unverified_draft

### bg-only-beta-1-3-oligomers-bind Dectin-1 lacks residues involved in calcium ligation that mediates carbohydrate-binding by classical C-type lectins, and among 187 diverse sequence-defined oligosaccharide probes together with designer microarrays from a neutral soluble glucan from S. cerevisiae, curdlan from Alcaligenes faecalis and pustulan from Umbilicaria papullosa, Dectin-1 binding is detected exclusively to 1,3-linked glucose oligomers, the minimum length required for detectable binding being a 10- or 11-mer, and 11-13 gluco-oligomers in clustered form displayed on liposomes mimic the macromolecular beta-glucans and compete with zymosan binding and triggering of tumour necrosis factor alpha secretion. 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 receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire. organism: Recombinant protein and a macrophage cell line tissue_or_cell_type: Cell-free microarray and cultured cells experimental_model: Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes limitations: A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line. exposure: Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan evidence_span: {"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"} [bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200

evidence_span

{"source_cache": "artifacts/glucan-research/15956283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c", "start_char": 0, "end_char": 990, "text_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c"}

experimental_model

Measurement of Syk activation and reactive oxygen production in macrophage subpopulations

exposure

Dectin-1 stimulation with assessment of Syk activation, reactive oxygen production and phagocytosis

limitations

The heterogeneity finding is the important limit: the pathway operated in a subpopulation in equilibrium with cells that could not use it, and the proportion shifted with cytokine treatment.

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

One kinase carries the oxidative burst but not the swallowing, and only some of the cells can run it at any moment.

primary_references

[bg-p15956283] Dectin-1 activates Syk tyrosine kinase in a dynamic subset of macrophages for reactive oxygen production. (2005). https://pubmed.ncbi.nlm.nih.gov/15956283/ DOI: 10.1182/blood-2005-03-1239

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 398–409

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Measurement of Syk activation and reactive oxygen production in macrophage subpopulations · source_derived_draft · unverified_draft

### bg-syk-carries-the-oxidative-burst Dectin-1 activates Syk in macrophages and is important for Dectin-1-stimulated reactive oxygen production but not for phagocytosis, Syk activation is restricted to a subpopulation of macrophages that is in equilibrium with cells that cannot activate the pathway, and the proportion of macrophages using this signalling pathway can be modulated by cytokine treatment, so Dectin-1 signalling reveals dynamic macrophage heterogeneity in inflammatory activation potential. 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: One kinase carries the oxidative burst but not the swallowing, and only some of the cells can run it at any moment. organism: Mouse tissue_or_cell_type: Macrophage experimental_model: Measurement of Syk activation and reactive oxygen production in macrophage subpopulations limitations: The heterogeneity finding is the important limit: the pathway operated in a subpopulation in equilibrium with cells that could not use it, and the proportion shifted with cytokine treatment. exposure: Dectin-1 stimulation with assessment of Syk activation, reactive oxygen production and phagocytosis evidence_span: {"source_cache": "artifacts/glucan-research/15956283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c", "start_char": 0, "end_char": 990, "text_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c"} [bg-p15956283] Dectin-1 activates Syk tyrosine kinase in a dynamic subset of macrophages for reactive oxygen production. (2005). https://pubmed.ncbi.nlm.nih.gov/15956283/ DOI: 10.1182/blood-2005-03-1239

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/glucan-research/19864672.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3", "start_char": 0, "end_char": 1842, "text_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3"}

experimental_model

Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled

exposure

Naturally occurring homozygous CARD9 Q295X premature termination, with reconstitution in Card9-null mouse myeloid cells

limitations

Human genetics with a linkage score of 3.6 and functional confirmation. It establishes the importance of the pathway in host defence; it says nothing about beta-glucan as a supplement.

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

People born without this one signalling protein get persistent fungal infections, which is how much the pathway matters.

primary_references

[bg-p19864672] A homozygous CARD9 mutation in a family with susceptibility to fungal infections. (2009). https://pubmed.ncbi.nlm.nih.gov/19864672/ DOI: 10.1056/nejmoa0810719

tissue_or_cell_type

Leukocytes

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 411–422

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled · source_derived_draft · unverified_draft

### bg-losing-card9-costs-antifungal-defence All four affected family members had a homozygous point mutation in CARD9 resulting in a premature termination codon Q295X, healthy family members had wild-type expression of the CARD9 protein while the four patients lacked wild-type expression which was associated with low numbers of interleukin-17-producing helper T cells, and functional studies based on genetic reconstitution of myeloid cells from Card9-null mice showed that the Q295X mutation impairs innate signalling from the antifungal pattern-recognition receptor dectin-1. 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: People born without this one signalling protein get persistent fungal infections, which is how much the pathway matters. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled limitations: Human genetics with a linkage score of 3.6 and functional confirmation. It establishes the importance of the pathway in host defence; it says nothing about beta-glucan as a supplement. exposure: Naturally occurring homozygous CARD9 Q295X premature termination, with reconstitution in Card9-null mouse myeloid cells evidence_span: {"source_cache": "artifacts/glucan-research/19864672.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3", "start_char": 0, "end_char": 1842, "text_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3"} [bg-p19864672] A homozygous CARD9 mutation in a family with susceptibility to fungal infections. (2009). https://pubmed.ncbi.nlm.nih.gov/19864672/ DOI: 10.1056/nejmoa0810719

evidence_span

{"source_cache": "artifacts/glucan-research/21525931.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0", "start_char": 0, "end_char": 1406, "text_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0"}

experimental_model

Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution

exposure

Soluble against particulate beta-glucan polymers on Dectin-1-expressing phagocytes

limitations

The abstract reports the soluble-versus-particulate comparison and the phosphatase exclusion. It does not state what happens when a soluble glucan is immobilised, 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

Mouse

plain_language

Binding was not enough: the receptor only fired when particles packed it into a patch that shut out the enzymes which switch it off.

primary_references

[bg-p21525931] Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. (2011). https://pubmed.ncbi.nlm.nih.gov/21525931/ DOI: 10.1038/nature10071

tissue_or_cell_type

Myeloid phagocytes

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 138–149

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution · source_derived_draft · unverified_draft

### bg-only-particles-signal Despite its ability to bind both soluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate beta-glucans, which cluster the receptor in synapse-like structures from which the regulatory tyrosine phosphatases CD45 and CD148 are excluded, providing a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance and initiate direct cellular antimicrobial responses only when they are required. 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: Binding was not enough: the receptor only fired when particles packed it into a patch that shut out the enzymes which switch it off. organism: Mouse tissue_or_cell_type: Myeloid phagocytes experimental_model: Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution limitations: The abstract reports the soluble-versus-particulate comparison and the phosphatase exclusion. It does not state what happens when a soluble glucan is immobilised, so no claim here rests on that. exposure: Soluble against particulate beta-glucan polymers on Dectin-1-expressing phagocytes evidence_span: {"source_cache": "artifacts/glucan-research/21525931.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0", "start_char": 0, "end_char": 1406, "text_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0"} [bg-p21525931] Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. (2011). https://pubmed.ncbi.nlm.nih.gov/21525931/ DOI: 10.1038/nature10071

evidence_span

{"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"}

experimental_model

Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients

exposure

Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody

limitations

A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment.

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

Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did.

primary_references

[bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265

tissue_or_cell_type

Relapsed or refractory high-risk neuroblastoma

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 346–357

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients · source_derived_draft · unverified_draft

### bg-dose-did-not-track-response One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response. 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: Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did. organism: Human tissue_or_cell_type: Relapsed or refractory high-risk neuroblastoma experimental_model: Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients limitations: A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment. exposure: Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody evidence_span: {"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"} [bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265

evidence_span

{"source_cache": "artifacts/glucan-research/36547975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2", "start_char": 0, "end_char": 2766, "text_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2"}

experimental_model

Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase

exposure

Oral beta-glucan during the first 5 weeks of GD2/GD3 vaccine priming against none, with all patients receiving glucan from week 6 onward

limitations

A randomised design that isolates one adjuvant window, with a prespecified type I error of 0.10 rather than the conventional 0.05. The endpoint is an antibody titre, not survival.

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

Starting the glucan earlier raised the antibody the vaccine was meant to raise, at a significance bar the trial had set in advance at one in ten.

primary_references

[bg-p36547975] Effect of Oral β-Glucan on Antibody Response to Ganglioside Vaccine in Patients With High-Risk Neuroblastoma: A Phase 2 Randomized Clinical Trial. (2023). https://pubmed.ncbi.nlm.nih.gov/36547975/ DOI: 10.1001/jamaoncol.2022.5999

tissue_or_cell_type

High-risk neuroblastoma

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 359–370

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase · source_derived_draft · unverified_draft

### bg-immunogenicity-in-genetic-responders Eligible patients receiving GD2/GD3 vaccine were randomly assigned to group 1 with 54 patients to receive no beta-glucan or group 2 with 53 patients to receive an oral beta-glucan regimen during the first 5 weeks of vaccine priming, and from week 6 onwards all 107 patients received oral beta-glucan during vaccine boost, adding oral beta-glucan during the first 5 weeks of vaccine priming elicited a higher anti-GD2 IgG1 antibody response in group 2 at 1.80 with 90% CI 0.12 to 3.39 and P = .08 against a planned type I error of 0.10, antibody titre correlated significantly with dectin-1 single nucleotide polymorphism, and the genotype frequency, seroconversion rates and vaccine-related toxic effects were similar in the 2 groups. 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: Starting the glucan earlier raised the antibody the vaccine was meant to raise, at a significance bar the trial had set in advance at one in ten. organism: Human tissue_or_cell_type: High-risk neuroblastoma experimental_model: Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase limitations: A randomised design that isolates one adjuvant window, with a prespecified type I error of 0.10 rather than the conventional 0.05. The endpoint is an antibody titre, not survival. exposure: Oral beta-glucan during the first 5 weeks of GD2/GD3 vaccine priming against none, with all patients receiving glucan from week 6 onward evidence_span: {"source_cache": "artifacts/glucan-research/36547975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2", "start_char": 0, "end_char": 2766, "text_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2"} [bg-p36547975] Effect of Oral β-Glucan on Antibody Response to Ganglioside Vaccine in Patients With High-Risk Neuroblastoma: A Phase 2 Randomized Clinical Trial. (2023). https://pubmed.ncbi.nlm.nih.gov/36547975/ DOI: 10.1001/jamaoncol.2022.5999

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

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

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/glucan-research/29246954.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6", "start_char": 0, "end_char": 1760, "text_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6"}

experimental_model

Physical, structural, purity, binding and functional comparison of five commercial laminarin preparations from three suppliers

exposure

Five laminarin preparations of molecular mass 4400 to 34,400 daltons, before and after extensive dialysis

limitations

Five preparations of one named natural product. Removing low molecular weight contaminants explained the behaviour of one preparation and not the others, so purity is one cause of the variation rather than the whole of it.

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 and mouse cells

plain_language

Five bottles with the same name on the label: two blocked the receptor, two switched it on, and cleaning up a fifth flipped it.

primary_references

[bg-p29246954] Immunoregulatory Activity of the Natural Product Laminarin Varies Widely as a Result of Its Physical Properties. (2018). https://pubmed.ncbi.nlm.nih.gov/29246954/ DOI: 10.4049/jimmunol.1701258

tissue_or_cell_type

Recombinant receptor and primary cells

trigger_kind

biomarker_context 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 164–175

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Physical, structural, purity, binding and functional comparison of five commercial laminarin preparations from three suppliers · source_derived_draft · unverified_draft

### bg-same-name-opposite-activity Laminarin is a (1->3, 1->6)-beta-glucan that is widely reported to be a Dectin-1 antagonist, however there are reports that laminarin is also a Dectin-1 agonist, and of five preparations from three commercial sources all contained laminarin although their molecular mass varied considerably from 4400 to 34,400 daltons, all were bound by recombinant human and mouse Dectin-1 but the affinity varied considerably and binding affinity did not correlate with Dectin-1 agonism, antagonism or potency, two laminarins were Dectin-1 antagonists and two were agonists, and the remaining laminarin was an antagonist but became an agonist when the low molecular weight moieties were removed. Condition category: biomarker_context 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: Five bottles with the same name on the label: two blocked the receptor, two switched it on, and cleaning up a fifth flipped it. organism: Human and mouse cells tissue_or_cell_type: Recombinant receptor and primary cells experimental_model: Physical, structural, purity, binding and functional comparison of five commercial laminarin preparations from three suppliers limitations: Five preparations of one named natural product. Removing low molecular weight contaminants explained the behaviour of one preparation and not the others, so purity is one cause of the variation rather than the whole of it. exposure: Five laminarin preparations of molecular mass 4400 to 34,400 daltons, before and after extensive dialysis evidence_span: {"source_cache": "artifacts/glucan-research/29246954.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6", "start_char": 0, "end_char": 1760, "text_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6"} [bg-p29246954] Immunoregulatory Activity of the Natural Product Laminarin Varies Widely as a Result of Its Physical Properties. (2018). https://pubmed.ncbi.nlm.nih.gov/29246954/ DOI: 10.4049/jimmunol.1701258

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/glucan-research/37515324.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f", "start_char": 0, "end_char": 1658, "text_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f"}

experimental_model

Glucan denaturation, fluorescence measurement of receptor aggregation and diffusion, and fungal particle contact sites

exposure

Fungal beta-glucans of low, medium and high molecular weight differing in helical structure content, before and after denaturation

limitations

A single-receptor-isoform study using defined glucan conformations. The aggregates observed were small, a few engaged receptors rather than synapse-scale structures.

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 receptor in cultured cells

plain_language

What decides whether the receptor fires is the shape the sugar holds in solution, not how tightly it sticks and not whether it dissolves.

primary_references

[bg-p37515324] Dectin-1 multimerization and signaling depends on fungal β-glucan structure and exposure. (2023). https://pubmed.ncbi.nlm.nih.gov/37515324/ DOI: 10.1016/j.bpj.2023.07.021

tissue_or_cell_type

Dectin-1A-expressing cells and Candida cell wall

trigger_kind

biomarker_context 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 151–162

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Glucan denaturation, fluorescence measurement of receptor aggregation and diffusion, and fungal particle contact sites · source_derived_draft · unverified_draft

### bg-structure-not-solubility-signals Beta-glucans can adopt solution structures ranging from random coil to insoluble fibre due to tertiary helical and quaternary structure, and despite similar affinity for Dectin-1 the ability of glucans to induce Dectin-1A-mediated signalling correlates with degree of structure, with glucan denaturation experiments showing that glucan structure determines agonistic potential but not receptor binding affinity, while fluorescence measurements provided direct evidence of ligation-induced Dectin-1A aggregation which positively correlated with increasing glucan structure content. Condition category: biomarker_context 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: What decides whether the receptor fires is the shape the sugar holds in solution, not how tightly it sticks and not whether it dissolves. organism: Human receptor in cultured cells tissue_or_cell_type: Dectin-1A-expressing cells and Candida cell wall experimental_model: Glucan denaturation, fluorescence measurement of receptor aggregation and diffusion, and fungal particle contact sites limitations: A single-receptor-isoform study using defined glucan conformations. The aggregates observed were small, a few engaged receptors rather than synapse-scale structures. exposure: Fungal beta-glucans of low, medium and high molecular weight differing in helical structure content, before and after denaturation evidence_span: {"source_cache": "artifacts/glucan-research/37515324.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f", "start_char": 0, "end_char": 1658, "text_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f"} [bg-p37515324] Dectin-1 multimerization and signaling depends on fungal β-glucan structure and exposure. (2023). https://pubmed.ncbi.nlm.nih.gov/37515324/ DOI: 10.1016/j.bpj.2023.07.021

evidence_span

{"source_cache": "artifacts/glucan-research/25258083.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872", "start_char": 0, "end_char": 1225, "text_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872"}

experimental_model

Histone modification profiling and genome-wide transcriptome of trained human monocytes, with pathway inhibition and a myeloid conditional knockout

exposure

Beta-glucan training with inhibition of Akt, mTOR or HIF-1 alpha, and metformin as an AMPK activator

limitations

The metformin result is an experimental inhibition of an induced response, not a clinical interaction study.

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 cells and mouse

plain_language

The rewiring costs energy: block the cell from burning glucose the fast way and the training does not take.

primary_references

[bg-p25258083] mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. (2014). https://pubmed.ncbi.nlm.nih.gov/25258083/ DOI: 10.1126/science.1250684

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 437–448

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Histone modification profiling and genome-wide transcriptome of trained human monocytes, with pathway inhibition and a myeloid conditional knockout · source_derived_draft · unverified_draft

### bg-training-needs-aerobic-glycolysis Trained monocytes display high glucose consumption, high lactate production and a high ratio of NAD+ to NADH, reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin through a dectin-1-Akt-HIF-1 alpha pathway, inhibition of Akt, mTOR or HIF-1 alpha blocked monocyte induction of trained immunity whereas the AMP-activated protein kinase activator metformin inhibited the innate immune response to fungal infection, and mice with a myeloid cell-specific defect in HIF-1 alpha were unable to mount trained immunity against bacterial sepsis. 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 rewiring costs energy: block the cell from burning glucose the fast way and the training does not take. organism: Human cells and mouse tissue_or_cell_type: Monocyte experimental_model: Histone modification profiling and genome-wide transcriptome of trained human monocytes, with pathway inhibition and a myeloid conditional knockout limitations: The metformin result is an experimental inhibition of an induced response, not a clinical interaction study. exposure: Beta-glucan training with inhibition of Akt, mTOR or HIF-1 alpha, and metformin as an AMPK activator evidence_span: {"source_cache": "artifacts/glucan-research/25258083.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872", "start_char": 0, "end_char": 1225, "text_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872"} [bg-p25258083] mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. (2014). https://pubmed.ncbi.nlm.nih.gov/25258083/ DOI: 10.1126/science.1250684

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