Evidence map›Paper›PMID 33343897›Full record

ArticleClinical & translational immunology2020

Innate lymphoid cell composition associates with COVID-19 disease severity.

Marina García, Efthymia Kokkinou, Anna Carrasco García, Tiphaine Parrot, Laura M Palma Medina, Kimia T Maleki, Wanda Christ, Renata Varnaitė, Iva Filipovic, Hans-Gustaf Ljunggren and 11 more

Open access · goldAbstract read
In one paragraph

Article in Clinical & translational immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. [Pulmonary innate immune response in Sars-cov-2 infection]Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2022
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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

21 authors at 1 institution in 1 country.

Marina GarcíaDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.ORCID https://orcid.org/0000-0002-9130-3933
Efthymia KokkinouDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.ORCID https://orcid.org/0000-0001-9248-4740
Anna Carrasco GarcíaDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Tiphaine ParrotDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Laura M Palma MedinaDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Kimia T MalekiDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Wanda ChristDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Renata VarnaitėDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Iva FilipovicDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Hans-Gustaf LjunggrenDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Niklas K BjörkströmDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Elin FolkessonDepartment of Infectious Diseases Karolinska University Hospital Stockholm Sweden.
Olav RooyackersDepartment of Clinical Science, Technology and Intervention Division of Anesthesiology and Intensive Care Karolinska Institutet Huddinge Sweden.
Lars I ErikssonFunction Perioperative Medicine and Intensive Care Karolinska University Hospital Stockholm Sweden.
Anders SönnerborgDepartment of Infectious Diseases Karolinska University Hospital Stockholm Sweden.
Soo AlemanDepartment of Infectious Diseases Karolinska University Hospital Stockholm Sweden.
Kristoffer StrålinDepartment of Infectious Diseases Karolinska University Hospital Stockholm Sweden.
Sara Gredmark-RussDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.
Jonas KlingströmDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.ORCID 0000-0001-9076-1441
Jenny MjösbergDepartment of Medicine Huddinge Center for Infectious Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden.ORCID https://orcid.org/0000-0002-1119-0976
Karolinska KI/K COVID‐19 Study Group
Karolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe role of innate lymphoid cells (ILCs) in coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is unknown. Understanding the immune response in COVID-19 could contribute to unravel the pathogenesis and identification of treatment targets. Here, we describe the phenotypic landscape of circulating ILCs in COVID-19 patients and identified ILC phenotypes correlated to serum biomarkers, clinical markers and laboratory parameters relevant in COVID-19.

methodsBlood samples collected from moderately (

resultsInnate lymphoid cells were largely depleted from the circulation of COVID-19 patients compared with healthy controls. Remaining circulating ILCs revealed decreased frequencies of ILC2 in severe COVID-19, with a concomitant decrease of ILC precursors (ILCp) in all patients, compared with controls. ILC2 and ILCp showed an activated phenotype with increased CD69 expression, whereas expression levels of the chemokine receptors CXCR3 and CCR4 were significantly altered in ILC2 and ILCp, and ILC1, respectively. The activated ILC profile of COVID-19 patients was associated with soluble inflammatory markers, while frequencies of ILC subsets were correlated with laboratory parameters that reflect the disease severity.

conclusionThis study provides insights into the potential role of ILCs in immune responses against SARS-CoV-2, particularly linked to the severity of COVID-19.

Indexed as

coronavirusCOVID‐19immune responseinnate lymphoid cellsrespiratory viral infectionSARS‐CoV‐2

Identifiers

PMID33343897
PMCPMC7734472
OpenAlexW3112988641

What OpenQuestion holds

Textmetadata
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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.