Component
The macrophage mannose receptor
The macrophage mannose receptor. 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.
Where it participates (unsigned role)
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.
Experimental context and source evidence
- 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
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
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.