Evidence map›Paper›PMID 34183391›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

IgA potentiates NETosis in response to viral infection.

Hannah D Stacey, Diana Golubeva, Alyssa Posca, Jann C Ang, Kyle E Novakowski, Muhammad Atif Zahoor, Charu Kaushic, Ewa Cairns, Dawn M E Bowdish, Caitlin E Mullarkey and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 59 citations in OpenAlex.

  1. SARS-CoV-2 Immune Complex-Mediated Neutrophil Activation.Open forum infectious diseases · 2025
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  16. The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 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

11 authors at 2 institutions in 1 country.

Hannah D StaceyMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Diana GolubevaMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Alyssa PoscaMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Jann C AngMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Kyle E NovakowskiMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Muhammad Atif ZahoorMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada, L8S 4K1.ORCID 0000-0003-2302-3689
Charu KaushicMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Ewa CairnsDepartment of Microbiology and Immunology, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada, N6A 3K7.ORCID 0000-0003-2748-3076
Dawn M E BowdishMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.ORCID 0000-0001-6823-2957
Caitlin E MullarkeyMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1.
Matthew S MillerMichael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada, L8S 4K1; mmiller@mcmaster.ca.ORCID 0000-0003-3426-5069
McMaster University · CAWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA is the second most abundant antibody present in circulation and is enriched at mucosal surfaces. As such, IgA plays a key role in protection against a variety of mucosal pathogens including viruses. In addition to neutralizing viruses directly, IgA can also stimulate Fc-dependent effector functions via engagement of Fc alpha receptors (Fc-αRI) expressed on the surface of certain immune effector cells. Neutrophils are the most abundant leukocyte, express Fc-αRI, and are often the first to respond to sites of injury and infection. Here, we describe a function for IgA-virus immune complexes (ICs) during viral infections. We show that IgA-virus ICs potentiate NETosis-the programmed cell-death pathway through which neutrophils release neutrophil extracellular traps (NETs). Mechanistically, IgA-virus ICs potentiated a suicidal NETosis pathway via engagement of Fc-αRI on neutrophils through a toll-like receptor-independent, NADPH oxidase complex-dependent pathway. NETs also were capable of trapping and inactivating viruses, consistent with an antiviral function.

Indexed as

AlphainfluenzavirusAntigen-Antibody ComplexAntigens, CDExtracellular TrapsHumansImmunoglobulin ANADPH OxidasesNeutrophilsReceptors, FcSARS-CoV-2Signal TransductionVirionVirus DiseasesAntigen-Antibody ComplexAntigens, CDFc(alpha) receptorImmunoglobulin ANADPH OxidasesReceptors, FcinfluenzaNETosisneutrophilsSARS-CoV-2viruses

Identifiers

PMID34183391
PMCPMC8271757
OpenAlexW3177484073

What OpenQuestion holds

Textmetadata
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.