Evidence map›Paper›PMID 34473802›Full record

ArticlePLoS pathogens2021

Neutrophils and lymphopenia, an unknown axis in severe COVID-19 disease.

Hernán F Peñaloza, Janet S Lee, Prabir Ray

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 43 citations in OpenAlex.

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  11. Host Response Changes and Their Association with Mortality in COVID-19 Patients with Lymphopenia.American journal of respiratory and critical care medicine · 2024
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  17. Severe COVID-19-associated hyperinflammatory syndrome versus classic hemophagocytic lymphohistiocytosis: similarities, differences, and the way forward.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2023
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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

3 authors at 1 institution in 1 country.

Hernán F PeñalozaAcute Lung Injury Center of Excellence, Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-1593-678X
Janet S LeeAcute Lung Injury Center of Excellence, Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-6812-6043
Prabir RayAcute Lung Injury Center of Excellence, Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
University of Pittsburgh · US

Funding

Regulation of Cardiolin Byosynthesis in Epithelial InjuryP01HL114453 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WATKINS, SIMON C · 2014 to 2023
$21.3M
Mechanisms of host protection against pathogen-secreted proteases in acute lung injuryR01HL136143 · NHLBI · WASHINGTON UNIVERSITY · PI LEE, JANET SOJUNG · 2017 to 2024
$4.4M
The role of ACOD1 in immunomodulation in intrapulmonary Klebsiella pneumoniae infectionR01HL142084 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, KONG · 2018 to 2021
$2.4M
Patient-Oriented Research in Acute Lung Injury and Host Defense in the ICUK24HL143285 · NHLBI · WASHINGTON UNIVERSITY · PI LEE, JANET SOJUNG · 2019 to 2023
$579k
NHLBI NIH HHS K24 HL143285NHLBI NIH HHS P01 HL114453NHLBI NIH HHS R01 HL136143NHLBI NIH HHS R01 HL142084
6 · The paper itself

Abstract

The Coronavirus Disease 2019 (COVID-19) is caused by the betacoronavirus Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus that can mediate asymptomatic or fatal infections characterized by pneumonia, acute respiratory distress syndrome (ARDS), and multi-organ failure. Several studies have highlighted the importance of B and T lymphocytes, given that neutralizing antibodies and T cell responses are required for an effective immunity. In addition, other reports have described myeloid cells such as macrophages and monocytes play a major role in the immunity against SARS-CoV-2 as well as dysregulated pro-inflammatory signature that characterizes severe COVID-19. During COVID-19, neutrophils have been defined as a heterogeneous group of cells, functionally linked to severe inflammation and thrombosis triggered by degranulation and NETosis, but also to suppressive phenotypes. The physiological role of suppressive neutrophils during COVID-19 and their implications in severe disease have been poorly studied and is not well understood. Here, we discuss the current evidence regarding the role of neutrophils with suppressive properties such as granulocytic myeloid-derived suppressor cells (G-MDSCs) and their possible role in suppressing CD4+ and CD8+ T lymphocytes expansion and giving rise to lymphopenia in severe COVID-19 infection.

Indexed as

AnimalsCOVID-19HumansLymphopeniaNeutrophilsSARS-CoV-2Severity of Illness Index

Identifiers

PMID34473802
PMCPMC8412274
OpenAlexW3197828661

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.