Evidence map›Paper›PMID 35095897›Full record

ArticleFrontiers in immunology2021

Spike-Dependent Opsonization Indicates Both Dose-Dependent Inhibition of Phagocytosis and That Non-Neutralizing Antibodies Can Confer Protection to SARS-CoV-2.

Wael Bahnan, Sebastian Wrighton, Martin Sundwall, Anna Bläckberg, Olivia Larsson, Urban Höglund, Hamed Khakzad, Magdalena Godzwon, Maria Walle, Elisabeth Elder and 12 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
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  5. T-Cell-Dependent Bispecific IgGs Protect Aged Mice From Lethal SARS-CoV-2 Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

22 authors at 4 institutions in 2 countries.

Wael BahnanDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Sebastian WrightonDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Martin SundwallDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Anna BläckbergDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Olivia LarssonAdlego Biomedical AB, Uppsala, Sweden.
Urban HöglundAdlego Biomedical AB, Uppsala, Sweden.
Hamed KhakzadEquipe Signalisation Calcique et Infections Microbiennes, Ecole Normale Supérieure Paris-Saclay, Gif-sur-Yvette, France.
Magdalena GodzwonDepartment of Immunotechnology, Lund University, Lund, Sweden.
Maria WalleDepartment of Immunotechnology, Lund University, Lund, Sweden.
Elisabeth ElderPublic Health Agency of Sweden, Solna, Sweden.
Anna Söderlund StrandDepartment of Laboratory Medicine, Clinical Microbiology, Skane University Hospital Lund, Lund University, Lund, Sweden.
Lotta HapponenDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Oscar AndréDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Johannes Kumra AhnlideDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Thomas HellmarkDepartment of Clinical Sciences Lund, Nephrology, Skane University Hospital Lund, Lund University, Lund, Sweden.
Vidar Wendel-HansenTanea Medical Ab, Uppsala, Sweden.
Robert Pa WallinSciEd Solutions, Stockholm, Sweden.
Johan MalmstömDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Lars MalmströmDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Mats OhlinDepartment of Immunotechnology, Lund University, Lund, Sweden.
Magnus RasmussenDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Pontus NordenfeltDepartment of Clinical Sciences Lund, Infection Medicine, Faculty of Medicine, Lund University, Lund, Sweden.
Lund University · SEInserm · FRPublic Health Agency of Sweden · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spike-specific antibodies are central to effective COVID19 immunity. Research efforts have focused on antibodies that neutralize the ACE2-Spike interaction but not on non-neutralizing antibodies. Antibody-dependent phagocytosis is an immune mechanism enhanced by opsonization, where typically, more bound antibodies trigger a stronger phagocyte response. Here, we show that Spike-specific antibodies, dependent on concentration, can either enhance or reduce Spike-bead phagocytosis by monocytes independently of the antibody neutralization potential. Surprisingly, we find that both convalescent patient plasma and patient-derived monoclonal antibodies lead to maximum opsonization already at low levels of bound antibodies and is reduced as antibody binding to Spike protein increases. Moreover, we show that this Spike-dependent modulation of opsonization correlate with the outcome in an experimental SARS-CoV-2 infection model. These results suggest that the levels of anti-Spike antibodies could influence monocyte-mediated immune functions and propose that non-neutralizing antibodies could confer protection to SARS-CoV-2 infection by mediating phagocytosis.

Indexed as

Antibodies, MonoclonalAntibodies, NeutralizingAntibodies, ViralCell LineCOVID-19HEK293 CellsHumansNeutralization TestsOpsonizationPhagocytosisSARS-CoV-2Spike Glycoprotein, CoronavirusAntibodies, MonoclonalAntibodies, NeutralizingAntibodies, ViralSpike Glycoprotein, Coronavirusantibodiesantibody bindingantibody functionin vivo modelphagocytosisSARS – CoV – 2spike (S) protein

Identifiers

PMID35095897
PMCPMC8796240
OpenAlexW4205417207

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.