Component

Complement component C3

Complement component C3. Species, exposure and limitations are retained in each linked claim.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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

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.

    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. 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.

    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

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