Component

Fc gamma receptor IIa / FCGR2A

Fc gamma receptor IIa / FCGR2A. Species, exposure and limitations are retained in each linked claim.

1 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. Imprime-induced anti-cancer functionality is dependent on immune complex formation with naturally-occurring anti-beta glucan antibodies, the formation of Imprime-antibody complexes activates complement primarily via the classical complement pathway and is opsonised by iC3b, immune complex binding depends upon Complement Receptor 3 and Fc gamma Receptor IIa eliciting phenotypic activation of and enhanced chemokine production by neutrophils and monocytes enabling these effector cells to kill antibody-opsonized tumour cells, and importantly these innate immune cell changes were not evident in subjects with low antibody levels but could be rescued with exogenous antibody supplementation.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/27812183.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf", "start_char": 0, "end_char": 1493, "text_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf"}
    experimental_model
    Whole blood from healthy human subjects with antibody-depleted and antibody-supplemented conditions
    exposure
    Imprime PGG in whole blood across a range of naturally occurring anti-beta-glucan antibody levels
    limitations
    Ex vivo whole blood rather than treated patients. The antibody dependence is demonstrated both by absence in low-antibody donors and by rescue with added antibody.
    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
    This soluble glucan does nothing on its own; it has to be caught by an antibody the person already had.
    primary_references
    [bg-p27812183] Imprime PGG-Mediated Anti-Cancer Immune Activation Requires Immune Complex Formation. (2016). https://pubmed.ncbi.nlm.nih.gov/27812183/ DOI: 10.1371/journal.pone.0165909
    tissue_or_cell_type
    Whole blood, neutrophil and 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 268–279

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole blood from healthy human subjects with antibody-depleted and antibody-supplemented conditions · source_derived_draft · unverified_draft

    ### bg-imprime-needs-an-antibody-first Imprime-induced anti-cancer functionality is dependent on immune complex formation with naturally-occurring anti-beta glucan antibodies, the formation of Imprime-antibody complexes activates complement primarily via the classical complement pathway and is opsonised by iC3b, immune complex binding depends upon Complement Receptor 3 and Fc gamma Receptor IIa eliciting phenotypic activation of and enhanced chemokine production by neutrophils and monocytes enabling these effector cells to kill antibody-opsonized tumour cells, and importantly these innate immune cell changes were not evident in subjects with low antibody levels but could be rescued with exogenous antibody supplementation. 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: This soluble glucan does nothing on its own; it has to be caught by an antibody the person already had. organism: Human tissue_or_cell_type: Whole blood, neutrophil and monocyte experimental_model: Whole blood from healthy human subjects with antibody-depleted and antibody-supplemented conditions limitations: Ex vivo whole blood rather than treated patients. The antibody dependence is demonstrated both by absence in low-antibody donors and by rescue with added antibody. exposure: Imprime PGG in whole blood across a range of naturally occurring anti-beta-glucan antibody levels evidence_span: {"source_cache": "artifacts/glucan-research/27812183.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf", "start_char": 0, "end_char": 1493, "text_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf"} [bg-p27812183] Imprime PGG-Mediated Anti-Cancer Immune Activation Requires Immune Complex Formation. (2016). https://pubmed.ncbi.nlm.nih.gov/27812183/ DOI: 10.1371/journal.pone.0165909
    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