The I-domain of CD11b: molecular mechanisms & dependencies

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.

Human evidence only

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)

CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated.
The lectin site of CD11b C-terminal to the I-domain → Beta-glucan source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"}
experimental_model
Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies
exposure
Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide
limitations
Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone.
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 complement receptor grips sugars at a second site, separate from the one that grips the complement fragment.
primary_references
[bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
tissue_or_cell_type
Leukocytes
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 203–214
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies · source_derived_draft · unverified_draft
### bg-cr3-has-a-lectin-site CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated. 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 complement receptor grips sugars at a second site, separate from the one that grips the complement fragment. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies limitations: Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone. exposure: Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide evidence_span: {"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"} [bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
Complete structured claim and evidence
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.
Beta-glucan → The primed state of complement receptor 3 source_derived_draftungraded
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
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 216–227
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.

The I-domain of CD11b