Evidence map›Paper›PMID 32971109›Full record

Trial reportThe Journal of allergy and clinical immunology2021

Elevated plasma sTIM-3 levels in patients with severe COVID-19.

Thor Ueland, Lars Heggelund, Andreas Lind, Aleksander R Holten, Kristian Tonby, Annika E Michelsen, Synne Jenum, Marthe J Jørgensen, Andreas Barratt-Due, Linda G Skeie and 16 more

Open access · bronzeAbstract readClinical TrialMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The Journal of allergy and clinical immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Novel insights into the effect of sTIM-3 on NLRP3 inflammasome via interacting with ASC.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  6. Article
  7. Review
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  9. TIM-3-driven macrophage polarisation is associated to recalcitrant chronic rhinosinusitis with nasal polyps.Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale · 2024
    Article
  10. Observational
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  14. Article
  15. Review
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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

26 authors at 4 institutions in 1 country.

Thor UelandResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway. Electronic address: thor.ueland@medisin.uio.no.
Lars HeggelundDepartment of Clinical Science, Faculty of Medicine, University of Bergen, Bergen, Norway; Department of Internal Medicine, Drammen Hospital, Drammen, Norway.
Andreas LindDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Aleksander R HoltenDivision of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway.
Kristian TonbyDepartment of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Annika E MichelsenResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Synne JenumDepartment of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Marthe J JørgensenInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Andreas Barratt-DueDivision of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway.
Linda G SkeieDepartment of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Ingvild NordøyResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Research Laboratory, Nordland Hospital, Bodø, Norway.
Mai Sasaki Aanensen FrazResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Else Quist-Paulsen EInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Microbiology, Oslo University Hospital, Oslo, Norway.
Søren E PischkeDivision of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway; Department of Immunology, University of Oslo, Oslo, Norway.
Simreen K JohalDepartment of Microbiology, Oslo University Hospital, Oslo, Norway.
Liv HesstvedtDepartment of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Mette BogenDepartment of Laboratory Medicine, Vestre Viken Hospital Trust, Drammen, Norway.
Børre FevangResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Bente HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Fredrik MüllerInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Microbiology, Oslo University Hospital, Oslo, Norway.
Gry Kloumann BekkenDepartment of Internal Medicine, Drammen Hospital, Drammen, Norway.
Tom E MollnesFaculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway; Department of Immunology, University of Oslo, Oslo, Norway; Research Laboratory, Nordland Hospital, Bodø, Norway; Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.
Susanne DudmanInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Microbiology, Oslo University Hospital, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Anne M Dyrhol-RiiseInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Jan C HolterInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Microbiology, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NODrammen Hospital · NOUniversity of Oslo · NOVestre Viken Hospital Trust · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathogenesis of coronavirus disease 2019 (COVID-19) is still incompletely understood, but it seems to involve immune activation and immune dysregulation.

objectiveWe examined the parameters of activation of different leukocyte subsets in COVID-19-infected patients in relation to disease severity.

methodsWe analyzed plasma levels of myeloperoxidase (a marker of neutrophil activation), soluble (s) CD25 (sCD25) and soluble T-cell immunoglobulin mucin domain-3 (sTIM-3) (markers of T-cell activation and exhaustion), and sCD14 and sCD163 (markers of monocyte/macrophage activation) in 39 COVID-19-infected patients at hospital admission and 2 additional times during the first 10 days in relation to their need for intensive care unit (ICU) treatment.

resultsOur major findings were as follows: (1) severe clinical outcome (ICU treatment) was associated with high plasma levels of sTIM-3 and myeloperoxidase, suggesting activated and potentially exhausted T cells and activated neutrophils, respectively; (2) in contrast, sCD14 and sCD163 showed no association with need for ICU treatment; and (3) levels of sCD25, sTIM-3, and myeloperoxidase were inversely correlated with degree of respiratory failure, as assessed by the ratio of Pao

conclusionOur findings suggest that neutrophil activation and, in particular, activated T cells may play an important role in the pathogenesis of COVID-19 infection, suggesting that T-cell-targeted treatment options and downregulation of neutrophil activation could be of importance in this disorder.

Indexed as

AgedAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCOVID-19FemaleHepatitis A Virus Cellular Receptor 2HumansInterleukin-2 Receptor alpha SubunitLipopolysaccharide ReceptorsLymphocyte ActivationMaleMiddle AgedReceptors, Cell SurfaceSARS-CoV-2Severity of Illness IndexAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2IL2RA protein, humanInterleukin-2 Receptor alpha SubunitLipopolysaccharide ReceptorsReceptors, Cell SurfaceCOVID-19neutrophiloutcomeT cellTIM-3

Identifiers

PMID32971109
PMCPMC7503135
OpenAlexW3087417377

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.