Evidence map›Paper›PMID 33096038›Full record

ArticleCurrent biology : CB2021

An Acquired and Endogenous Glycocalyx Forms a Bidirectional "Don't Eat" and "Don't Eat Me" Barrier to Phagocytosis.

Paul R C Imbert, Amra Saric, Kayvon Pedram, Carolyn R Bertozzi, Sergio Grinstein, Spencer A Freeman

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in Current biology : CB, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Airway macrophage specific glycocalyx expression and remodeling following viral infection.Matrix biology : journal of the International Society for Matrix Biology · 2026
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  11. The physical landscape of CAR-T synapse.Biophysical journal · 2024
    Review
  12. Phagocytosis Checkpoints in Glioblastoma: CD47 and Beyond.Current issues in molecular biology · 2024
    Review
  13. Article
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  19. Review
  20. Targeted glycan degradation potentiates cellular immunotherapy for solid tumors.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 6 institutions in 2 countries.

Paul R C ImbertProgram in Cell Biology, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children, 686 Bay Street, 19-9800, Toronto, ON M5G 0A4, Canada.
Amra SaricNeurosciences and Cellular and Structural Biology Division, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Kayvon PedramDepartment of Chemistry and Stanford ChEM-H, Stanford University, Stanford, CA 94305, USA.
Carolyn R BertozziDepartment of Chemistry and Stanford ChEM-H, Stanford University, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford, CA 94305, USA.
Sergio GrinsteinProgram in Cell Biology, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children, 686 Bay Street, 19-9800, Toronto, ON M5G 0A4, Canada; Department of Biochemistry, University of Toronto, Toronto, ON, Canada; Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON M5B 1W8, Canada. Electronic address: sergio.grinstein@sickkids.ca.
Spencer A FreemanProgram in Cell Biology, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children, 686 Bay Street, 19-9800, Toronto, ON M5G 0A4, Canada; Department of Biochemistry, University of Toronto, Toronto, ON, Canada. Electronic address: spencer.freeman@sickkids.ca.
Hospital for Sick Children · CAHoward Hughes Medical Institute · USNational Institutes of Health · USStanford University · USSt. Michael's Hospital · CAUniversity of Toronto · CA

Funding

Targeting the Cancer GlycocalyxR01CA227942 · NCI · STANFORD UNIVERSITY · PI Carolyn Bertozzi · 2019 to 2026
$3.6M
Stanford Chem-H Chemistry/Biology Interface Predoctoral Training ProgramT32GM120007 · NIGMS · STANFORD UNIVERSITY · PI BERTOZZI, CAROLYN · 2016 to 2020
$1.2M
CIHR FDN-143202NCI NIH HHS R01 CA227942NIGMS NIH HHS T32 GM120007
6 · The paper itself

Abstract

Macrophages continuously survey their environment in search of pathogens or apoptotic corpses or debris. Targets intended for clearance expose ligands that initiate their phagocytosis ("eat me" signals), while others avoid phagocytosis by displaying inhibitory ligands ("don't eat me" signals). We report that such ligands can be obscured by the glycosaminoglycans and glycoproteins that coat pathogenic as well as malignant phagocytic targets. In addition, a reciprocal barrier of self-synthesized or acquired glycocalyx components on the macrophage surface shrouds phagocytic receptors, curtailing their ability to engage particles. The coating layers of macrophages and their targets hinder phagocytosis by both steric and electrostatic means. Their removal by enzymatic means is shown to markedly enhance phagocytic efficiency. In particular, we show that the removal of mucins, which are overexpressed in cancer cells, facilitates their clearance. These results shed light on the physical barriers that modulate phagocytosis, which have been heretofore underappreciated. VIDEO ABSTRACT.

Indexed as

AdultAnimalsBiological ProductsCandida albicansCandidiasis, InvasiveCD47 AntigenDisease Models, AnimalFemaleGlycocalyxGlycosaminoglycansHealthy VolunteersHumansHyaluronic AcidImmunoglobulin GMacrophagesMaleBiological ProductsCD47 AntigenGlycosaminoglycansHyaluronic AcidImmunoglobulin GMucinsCandida albicansCD47hyaluronanmucinasesialic acidsurface chargesyndecansynovial-resident macrophagestumor-associated macrophages

Identifiers

PMID33096038
PMCPMC7855322
OpenAlexW3094318117

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.