Component
The phagocytic synapse, a receptor-rich contact that excludes CD45 and CD148
The phagocytic synapse, a receptor-rich contact that excludes CD45 and CD148. 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 it acts on
Despite its ability to bind both soluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate beta-glucans, which cluster the receptor in synapse-like structures from which the regulatory tyrosine phosphatases CD45 and CD148 are excluded, providing a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance and initiate direct cellular antimicrobial responses only when they are required.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/21525931.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0", "start_char": 0, "end_char": 1406, "text_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0"}
- experimental_model
- Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution
- exposure
- Soluble against particulate beta-glucan polymers on Dectin-1-expressing phagocytes
- limitations
- The abstract reports the soluble-versus-particulate comparison and the phosphatase exclusion. It does not state what happens when a soluble glucan is immobilised, so no claim here rests on that.
- 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
- Binding was not enough: the receptor only fired when particles packed it into a patch that shut out the enzymes which switch it off.
- primary_references
- [bg-p21525931] Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. (2011). https://pubmed.ncbi.nlm.nih.gov/21525931/ DOI: 10.1038/nature10071
- tissue_or_cell_type
- Myeloid phagocytes
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution · source_derived_draft · unverified_draft
### bg-only-particles-signal Despite its ability to bind both soluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate beta-glucans, which cluster the receptor in synapse-like structures from which the regulatory tyrosine phosphatases CD45 and CD148 are excluded, providing a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance and initiate direct cellular antimicrobial responses only when they are required. 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: Binding was not enough: the receptor only fired when particles packed it into a patch that shut out the enzymes which switch it off. organism: Mouse tissue_or_cell_type: Myeloid phagocytes experimental_model: Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution limitations: The abstract reports the soluble-versus-particulate comparison and the phosphatase exclusion. It does not state what happens when a soluble glucan is immobilised, so no claim here rests on that. exposure: Soluble against particulate beta-glucan polymers on Dectin-1-expressing phagocytes evidence_span: {"source_cache": "artifacts/glucan-research/21525931.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0", "start_char": 0, "end_char": 1406, "text_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0"} [bg-p21525931] Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. (2011). https://pubmed.ncbi.nlm.nih.gov/21525931/ DOI: 10.1038/nature10071
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.