Evidence map›Paper›PMID 41058707›Full record

ArticleFrontiers in immunology2025

Identification of blood immunological biomarkers of SARS-CoV-2 infection during pandemic in Poland.

Monika Leśniak, Agata Borkowska, Krzysztof Kłos, Karolina Aleksandrowicz, Klaudia Porębska, Dagmara Kobza, Krzysztof Łukasz Piwowarek, Katarzyna Plewka-Barcik, Marcin Niemcewicz, Anna Lutyńska and 3 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Immune Dysregulation After COVID-19: Longitudinal Analysis up to 9 Months.International journal of molecular sciences · 2026
    Article
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

13 authors.

Monika Leśniak *Laboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Agata Borkowska *Laboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Krzysztof KłosDepartment of Internal Medicine, Infectious Diseases and Allergology, Military Institute of Medicine- National Research Institute, Warsaw, Poland.
Karolina AleksandrowiczLaboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Klaudia PorębskaLaboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Dagmara KobzaLaboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Krzysztof Łukasz PiwowarekDepartment of Internal Medicine, Infectious Diseases and Allergology, Military Institute of Medicine- National Research Institute, Warsaw, Poland.
Katarzyna Plewka-BarcikDepartment of Internal Medicine, Infectious Diseases and Allergology, Military Institute of Medicine- National Research Institute, Warsaw, Poland.
Marcin NiemcewiczBiohazard Prevention Centre, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Anna LutyńskaLaboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Jacek Z KubiakLaboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.
Andrzej ChciałowskiDepartment of Internal Medicine, Infectious Diseases and Allergology, Military Institute of Medicine- National Research Institute, Warsaw, Poland.
Robert ZdanowskiLaboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine-National Research Institute, Warsaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intoduction: T lymphocytes, along with cytokines and chemokines-dependent pathways are primarily responsible for regulating the immune response, controlling inflammation and eliminating viral infections. However, excessive immune activity can lead to pathological effects such as cytokine storm, which may cause severe respiratory distress syndrome and multi-organ damage in COVID-19. The aim of this study was to identify potential biomarkers of SARS-CoV-2 infection that could predict the severity of COVID-19 progression. Methods: The cohort in this study included 52 hospitalized adult patients with SARS-CoV-2 infection from Warsaw, Poland admitted to the hospital during COVID-19 pandemic (February to November 2021). Based on clinical symptoms, patients were divided into two groups: (i) mild/moderate symptoms (non-severe) - 44 patients and (ii) severe respiratory failure (severe) - 8 patients. The control group consisted of 26 individuals without COVID-19. All COVID-19 patients and healthy controls underwent immunophenotyping of peripheral blood to assess the abundance of T lymphocytes and regulatory T lymphocytes, as well as measurement of selected cytokine and chemokine concentrations in corresponding serum samples. Data analysis was performed using CytoFLEX Flow Cytometer. Results and discussion: Decreased percentages of total lymphocytes and T lymphocytes in peripheral blood were observed across all COVID-19 patients, with varying degrees between the non-severe and severe groups. A significant reduction was also noted in double-positive lymphocytes (CD4+CD8+), regulatory T lymphocytes ( CD4+ CD25HiCD127Lo and CD4+CD25HiCD127LoFoxP3+), as well as CD4+CD25+/-, CD4+CD45RA+/-, and CD8+CD45RA+/- subsets. Elevated levels of IL-6, IL-10, IL-17A, IFN-g, CCL2, CXCL8, and CXCL10 were observed in the non-severe and/or severe groups compared to healthy controls. Most importantly, only CXCL10 was significantly elevated in the severe group at admission compared to the non-severe group. In this study, we identified the chemokine CXCL10 as a crucial marker for distinguishing the severe course of COVID-19 from non-severe form at the time of admission. It may serve as an early indicator of diseases progression during hospitalization, potentially allowing prediction of the disease course. Moreover, elevated CXCL10 levels, in combination with decreased total lymphocytes counts and increased levels of IL-6, IL10, IFNg, CCL2 and CXCL9, may represent a more comprehensive biomarker panel suitable for predicting the severity of COVID-19.

Indexed as

COVID-19SARS-CoV-2AdultAgedBiomarkersCytokinesFemaleHumansMaleMiddle AgedPandemicsPolandSeverity of Illness IndexT-Lymphocytes, RegulatoryBiomarkersCytokinesbiomarkersCOVID-19CXCL10pandemicSARS-CoV-2severityT lymphocytes

Identifiers

PMID41058707
PMCPMC12497783

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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.