Component
The primed state of complement receptor 3
The primed state of complement receptor 3. 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"}
- experimental_model
- Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets
- exposure
- Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar
- limitations
- An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Human
- plain_language
- The sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill.
- primary_references
- [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777
- tissue_or_cell_type
- Neutrophil and natural killer cell
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets · source_derived_draft · unverified_draft
### bg-soluble-glucan-primes-cr3 When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill. organism: Human tissue_or_cell_type: Neutrophil and natural killer cell experimental_model: Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets limitations: An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient. exposure: Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar evidence_span: {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"} [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.