Evidence map›Paper›PMID 35690570›Full record

ArticleEuropean journal of internal medicine2022

T-cell immune response predicts the risk of critical SARS-Cov2 infection in hospitalized COVID-19 patients.

Maxime Samson, Barbara Nicolas, Marion Ciudad, Hélène Greigert, Alexandre Guilhem, Claudie Cladiere, Cécile Straub, Mathieu Blot, Lionel Piroth, Thomas Rogier and 7 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in European journal of internal medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04410432 (Immune Response and Risk of Serious Infection to SARS-Cov2), which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 26% 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.

NCT04410432 completednot on this map

Immune Response and Risk of Serious Infection to SARS-Cov2

TypeobservationalSponsorCentre Hospitalier Universitaire DijonRan2020 to 2021Enrolled39ConditionsSARS Cov2, Immune ResponseArmsBlood sample collection
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

17 authors at 2 institutions in 1 country.

Maxime SamsonDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France. Electronic address: maxime.samson@chu-dijon.fr.
Barbara NicolasDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Marion CiudadDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Hélène GreigertDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Alexandre GuilhemDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Claudie CladiereDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Cécile StraubDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Mathieu BlotDepartment of Infectious diseases, University Hospital of DijonDijon, France.
Lionel PirothDepartment of Infectious diseases, University Hospital of DijonDijon, France.
Thomas RogierDepartment of internal medicine and systemic diseases, University Hospital of DijonDijon, France.
Hervé DevilliersDepartment of internal medicine and systemic diseases, University Hospital of DijonDijon, France.
Patrick ManckoundiaDepartment of geriatric internal medicine, University Hospital of DijonDijon, France.
Thibault GhesquiereDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Stéphanie FrancoisLaboratory of immunology, University Hospital of DijonDijon, France.
Daniela LakomyLaboratory of immunology, University Hospital of DijonDijon, France.
Sylvain AudiaDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Bernard BonnotteDepartment of Internal Medicine and Clinical Immunology, University Hospital of Dijon; INSERM U1098, University of Bourgogne-Franche Comté, Dijon, France.
Inserm · FRMaison des Sciences sociales et des Humanités de Dijon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThis study aimed to identify markers of disease worsening in patients hospitalized for SARS-Cov2 infection. PATIENTS AND

methodsPatients hospitalized for severe recent-onset (<1 week) SARS-Cov2 infection were prospectively included. The percentage of T-cell subsets and plasma IL-6 at admission (before any steroid therapy) were compared between patients who progressed to a critical infection and those who did not.

resultsThirty-seven patients (18 men, 19 women) were included; 11 (30%) progressed to critical infection. At admission, the critical infection patients were older (P = 0.021), had higher creatinine levels (P = 0.003), and decreased percentages of circulating B cells (P = 0.04), T cells (P = 0.009), and CD4+ T cells (P = 0.004) than those with a favorable course. Among T cell subsets, there was no significant difference between the two groups except for the percentage of Th17 cells, which was two-fold higher in patients who progressed to critical infection (P = 0.028). Plasma IL-6 at admission was also higher in this group (P = 0.018). In multivariate analysis, the percentage of circulating Th17 cells at admission was the only variable associated with higher risk of progression to critical SARS-Cov2 infection (P = 0.021).

conclusionThis study suggests that an elevated percentage of Th17 cells in patients hospitalized for SARS-Cov2 infection is associated with an increased risk of progression to critical disease. If these data are confirmed in a larger study, this marker could be used to better target the population of patients in whom tocilizumab could decrease the risk of progression to critical COVID-19.

Indexed as

COVID-19FemaleHumansImmunityInterleukin-6MaleRNA, ViralSARS-CoV-2T-LymphocytesInterleukin-6RNA, ViralCovid-19IL-6SARS Cov2Th17 cells

Identifiers

PMID35690570
PMCPMC9163020
OpenAlexW4281748826

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.