Evidence map›Paper›PMID 23964276›Full record

ArticleFrontiers in immunology2013

Binding of Soluble Yeast β-Glucan to Human Neutrophils and Monocytes is Complement-Dependent.

Nandita Bose, Anissa S H Chan, Faimola Guerrero, Carolyn M Maristany, Xiaohong Qiu, Richard M Walsh, Kathleen E Ertelt, Adria Bykowski Jonas, Keith B Gorden, Christine M Dudney and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 61 citations in OpenAlex.

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  7. Frontiers in nutrition · 2025
    Article
  8. Article
  9. Review
  10. β-glucans fromFrontiers in nutrition · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Effects of Medicinal Fungi-Derived β-Glucan on Tumor Progression.Journal of fungi (Basel, Switzerland) · 2021
    Review
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Nandita BoseBiothera , Eagan, MN , USA.
Anissa S H Chan
Faimola Guerrero
Carolyn M Maristany
Xiaohong Qiu
Richard M Walsh
Kathleen E Ertelt
Adria Bykowski Jonas
Keith B Gorden
Christine M Dudney
Lindsay R Wurst
Michael E Danielson
Natalie Elmasry
Andrew S Magee
Myra L Patchen
John P Vasilakos
ProThera Biologics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immunomodulatory properties of yeast β-1,3/1,6 glucans are mediated through their ability to be recognized by human innate immune cells. While several studies have investigated binding of opsonized and unopsonized particulate β-glucans to human immune cells mainly via complement receptor 3 (CR3) or Dectin-1, few have focused on understanding the binding characteristics of soluble β-glucans. Using a well-characterized, pharmaceutical-grade, soluble yeast β-glucan, this study evaluated and characterized the binding of soluble β-glucan to human neutrophils and monocytes. The results demonstrated that soluble β-glucan bound to both human neutrophils and monocytes in a concentration-dependent and receptor-specific manner. Antibodies blocking the CD11b and CD18 chains of CR3 significantly inhibited binding to both cell types, establishing CR3 as the key receptor recognizing the soluble β-glucan in these cells. Binding of soluble β-glucan to human neutrophils and monocytes required serum and was also dependent on incubation time and temperature, strongly suggesting that binding was complement-mediated. Indeed, binding was reduced in heat-inactivated serum, or in serum treated with methylamine or in serum reacted with the C3-specific inhibitor compstatin. Opsonization of soluble β-glucan was demonstrated by detection of iC3b, the complement opsonin on β-glucan-bound cells, as well as by the direct binding of iC3b to β-glucan in the absence of cells. Binding of β-glucan to cells was partially inhibited by blockade of the alternative pathway of complement, suggesting that the C3 activation amplification step mediated by this pathway also contributed to binding.

Indexed as

C3CR3monocytesneutrophilsopsonizationβ-glucans

Identifiers

PMID23964276
PMCPMC3740326
OpenAlexW1968596651

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.