Granulocyte

Where it participates (unsigned role)

1. Recent data indicated that barley beta-1,3;1,4-glucan given orally potentiated the activity of antitumour monoclonal antibody leading to enhanced tumour regression and survival, and this investigation showed that orally administered yeast beta-1,3;1,6-glucan functioned similarly to barley beta-1,3;1,4-glucan with antitumour monoclonal antibody, with both oral beta-1,3-glucans a requirement for iC3b on tumours and CR3 on granulocytes being confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3.

   Barley mixed-linkage beta-(1->3)/(1->4)-glucan → Yeast beta-(1->3)/(1->6)-glucan source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   machinery_impairment Imported condition classification; unverified.

   evidence_span

   {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"}

   experimental_model

   Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice

   exposure

   Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody

   limitations

   The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people.

   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

   A cereal glucan and a yeast glucan did the same job by the same route, which is the result that refuses to let the two be filed apart.

   primary_references

   [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797

   tissue_or_cell_type

   Gut, spleen, lymph node, bone marrow and tumour

   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 242–253

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice · source_derived_draft · unverified_draft

   ### bg-barley-and-yeast-converge Recent data indicated that barley beta-1,3;1,4-glucan given orally potentiated the activity of antitumour monoclonal antibody leading to enhanced tumour regression and survival, and this investigation showed that orally administered yeast beta-1,3;1,6-glucan functioned similarly to barley beta-1,3;1,4-glucan with antitumour monoclonal antibody, with both oral beta-1,3-glucans a requirement for iC3b on tumours and CR3 on granulocytes being confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3. 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: A cereal glucan and a yeast glucan did the same job by the same route, which is the result that refuses to let the two be filed apart. organism: Mouse tissue_or_cell_type: Gut, spleen, lymph node, bone marrow and tumour experimental_model: Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice limitations: The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people. exposure: Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody evidence_span: {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"} [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797

   Complete structured claim and evidence

2. Barley and yeast beta-1,3-glucan were labelled with fluorescein to track their oral uptake and processing in vivo, orally administered beta-1,3-glucans were taken up by macrophages that transported them to spleen, lymph nodes and bone marrow, within the bone marrow the macrophages degraded the large beta-1,3-glucans into smaller soluble beta-1,3-glucan fragments that were taken up by the CR3 of marginated granulocytes, and these granulocytes with CR3-bound beta-1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumour cells following their recruitment to a site of complement activation resembling a tumour coated with monoclonal antibody.

   Transport of ingested glucan by macrophages to spleen, lymph node and marrow → Beta-(1->3)-linked gluco-oligosaccharides source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"}

   experimental_model

   Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice

   exposure

   Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody

   limitations

   The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people.

   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

   Swallowed glucan is carried to the marrow inside macrophages, cut up there, and handed to granulocytes on the way out.

   primary_references

   [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797

   tissue_or_cell_type

   Gut, spleen, lymph node, bone marrow and tumour

   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 255–266

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice · source_derived_draft · unverified_draft

   ### bg-macrophages-carry-and-cut-it Barley and yeast beta-1,3-glucan were labelled with fluorescein to track their oral uptake and processing in vivo, orally administered beta-1,3-glucans were taken up by macrophages that transported them to spleen, lymph nodes and bone marrow, within the bone marrow the macrophages degraded the large beta-1,3-glucans into smaller soluble beta-1,3-glucan fragments that were taken up by the CR3 of marginated granulocytes, and these granulocytes with CR3-bound beta-1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumour cells following their recruitment to a site of complement activation resembling a tumour coated with monoclonal antibody. 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: Swallowed glucan is carried to the marrow inside macrophages, cut up there, and handed to granulocytes on the way out. organism: Mouse tissue_or_cell_type: Gut, spleen, lymph node, bone marrow and tumour experimental_model: Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice limitations: The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people. exposure: Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody evidence_span: {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"} [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797

   Complete structured claim and evidence

3. 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