Evidence map›Paper›PMID 42712717›Full record

ArticleFrontiers in immunology2026

Induction of dysfunctional CD14

Salimeh Ebrahimnezhaddarzi, Aimee Altermatt, Hans Kek, Jingling Zhou, Irene Boo, James H McMahon, Bradley J Gardiner, Rachel Sacks-Davis, Heidi E Drummer, Anthony Jaworowski and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Salimeh EbrahimnezhaddarziDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
Aimee AltermattDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
Hans KekDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
Jingling ZhouSchool of Health and Biomedical Sciences, RMIT University, Melbourne, VIC, Australia.
Irene BooDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
James H McMahonDepartment of Infectious Diseases, The Alfred Hospital and Monash University, Melbourne, VIC, Australia.
Bradley J GardinerDepartment of Infectious Diseases, The Alfred Hospital and Monash University, Melbourne, VIC, Australia.
Rachel Sacks-DavisDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
Heidi E DrummerDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
Anthony JaworowskiDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.
Anna C HearpsDisease Elimination Program, Burnet Institute, Melbourne, VIC, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Severe COVID-19 disease is characterised by a state of hyperinflammation. As key producers of inflammatory mediators in blood, altered inflammatory activity of monocytes within some individuals may contribute to adverse disease outcomes. Methods: Analysis of monocyte activity under settings of infection and inflammation can be challenged by activation-induced shedding of monocyte receptors traditionally used to identify monocyte subsets. Here, we utilised alternative, more robust immunophenotyping approaches to investigate the impact of COVID-19 infection on monocyte phenotype and inflammatory status. Results: Immunophenotype analysis of cryopreserved peripheral blood mononuclear cells from unvaccinated, previously COVID-19 naive individuals (median age 43 years, range 21-95, n=42) with a PCR-confirmed acute COVID-19 infection indicated expansion of a novel population of CD14 Discussion: COVID-19 is associated with expansion of a novel subset of monocytes with impaired inflammatory activity that persist for at least 3 months after acute infection. Whether this population is uniquely expanded by COVID-19, and the long term implications of its persistence post-acute disease, remain to be defined.

Indexed as

COVID-19Lipopolysaccharide ReceptorsMonocytesSARS-CoV-2AdultAgedAged, 80 and overCytokinesFemaleGPI-Linked ProteinsHumansImmunophenotypingMaleMiddle AgedReceptors, IgGYoung AdultCD14 protein, humanCytokinesFCGR3B protein, humanGPI-Linked ProteinsLipopolysaccharide ReceptorsReceptors, IgGCD14COVID-19inflammatory responsemonocytemonocyte subsets

Identifiers

PMID42712717
PMCPMC13550204

What OpenQuestion holds

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Registered trials

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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.