Evidence map›Paper›PMID 33492309›Full record

ArticleThe Journal of clinical investigation2021

Functional monocytic myeloid-derived suppressor cells increase in blood but not airways and predict COVID-19 severity.

Sara Falck-Jones, Sindhu Vangeti, Meng Yu, Ryan Falck-Jones, Alberto Cagigi, Isabella Badolati, Björn Österberg, Maximilian Julius Lautenbach, Eric Åhlberg, Ang Lin and 12 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06401720 (Respiratory Immune Responses in Human Influenza Virus Infection Across Age to Understand What Dictates Disease Severity), which is not on this map. Cited by 82 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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.

NCT06401720 enrolling by invitationnot on this mapstarted 2024, after this paper: background citation

Respiratory Immune Responses in Human Influenza Virus Infection Across Age to Understand What Dictates Disease Severity

TypeobservationalSponsorKarolinska InstitutetRan2024 to 2030Enrolled800ConditionsInfluenza A Infection, Influenza B Virus Infection, SARS CoV 2 Infection, RSV Infection
3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Innate immunity to SARS-CoV-2 infection: a review.Epidemiology and infection · 2022
    Pooled it
  3. Trial
  4. Article
  5. Review
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  8. Article
  9. Review
  10. Article
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  13. Article
  14. The CD38Frontiers in immunology · 2025
    Article
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  17. Review
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  20. Review

22 more citing papers are in PubMed but not listed here.

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.

Sara Falck-JonesDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Sindhu VangetiDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Meng YuDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Ryan Falck-JonesDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Alberto CagigiDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Isabella BadolatiDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Björn ÖsterbergDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Maximilian Julius LautenbachDivision of Infectious Diseases, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Eric ÅhlbergDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Ang LinDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Rico LepzienDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Inga SzurgotDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Klara LenartDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Fredrika HellgrenDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Holden MaeckerStanford University Medical Center, Stanford, California, USA.
Jörgen SäldeHealth Care Services Stockholm County (SLSO), Stockholm, Sweden.
Jan AlbertDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Niclas JohanssonDivision of Infectious Diseases, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Max BellDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Karin LoréDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Anna FärnertDivision of Infectious Diseases, Department of Medicine Solna, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Anna Smed-SörensenDivision of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Karolinska University Hospital · SEKarolinska Institutet · SEStanford Medicine · USStockholm Health Care Services · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immunopathology of coronavirus disease 2019 (COVID-19) remains enigmatic, causing immunodysregulation and T cell lymphopenia. Monocytic myeloid-derived suppressor cells (M-MDSCs) are T cell suppressors that expand in inflammatory conditions, but their role in acute respiratory infections remains unclear. We studied the blood and airways of patients with COVID-19 across disease severities at multiple time points. M-MDSC frequencies were elevated in blood but not in nasopharyngeal or endotracheal aspirates of patients with COVID-19 compared with healthy controls. M-MDSCs isolated from patients with COVID-19 suppressed T cell proliferation and IFN-γ production partly via an arginase 1-dependent (Arg-1-dependent) mechanism. Furthermore, patients showed increased Arg-1 and IL-6 plasma levels. Patients with COVID-19 had fewer T cells and downregulated expression of the CD3ζ chain. Ordinal regression showed that early M-MDSC frequency predicted subsequent disease severity. In conclusion, M-MDSCs expanded in the blood of patients with COVID-19, suppressed T cells, and were strongly associated with disease severity, indicating a role for M-MDSCs in the dysregulated COVID-19 immune response.

Indexed as

AdultAgedAged, 80 and overArginaseCase-Control StudiesCohort StudiesCOVID-19FemaleHumansInfluenza, HumanInterferon-gammaInterleukin-6Leukocyte CountMaleMiddle AgedMyeloid-Derived Suppressor CellsARG1 protein, humanArginaseIL6 protein, humanInterferon-gammaInterleukin-6COVID-19ImmunologyInnate immunity

Identifiers

PMID33492309
PMCPMC7954608
OpenAlexW3121940444

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Registered trials

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.