Evidence map›Paper›PMID 38804979›Full record

ArticleEmerging microbes & infections2024

SARS-CoV-2 infection induces adaptive NK cell responses by spike protein-mediated induction of HLA-E expression.

Mohammad Zahidul Hasan, Maren Claus, Nadine Krüger, Sarah Reusing, Eline Gall, Christina Bade-Döding, Armin Braun, Carsten Watzl, Markus Uhrberg, Lutz Walter

Abstract read
In one paragraph

Article in Emerging microbes & infections, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. NK Cells: A Powerful Squad Versus SARS-CoV-2.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
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

10 authors.

Mohammad Zahidul HasanPrimate Genetics Laboratory, German Primate Center, Leibniz-Institute for Primate Research, Göttingen, Germany.
Maren ClausDepartment for Immunology, Leibniz Research Centre for Working Environment and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Nadine KrügerPlatform Infection Models, German Primate Center, Leibniz-Institute for Primate Research, Göttingen, Germany.ORCID 0000-0002-4413-8699
Sarah ReusingInstitute for Transplantation Diagnostics and Cell Therapeutics, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Eline GallInstitute for Transfusion Medicine, Hannover Medical School, Hannover, Germany.
Christina Bade-DödingInstitute for Transfusion Medicine, Hannover Medical School, Hannover, Germany.
Armin BraunFraunhofer Institute for Toxicology and Experimental Medicine, Member of the German Center for Lung Research (DZL), Biomedical Research in Endstage and Obstructive Lung Disease (BREATH), Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.
Carsten WatzlDepartment for Immunology, Leibniz Research Centre for Working Environment and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Markus UhrbergInstitute for Transplantation Diagnostics and Cell Therapeutics, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.ORCID 0000-0001-9553-1987
Lutz WalterPrimate Genetics Laboratory, German Primate Center, Leibniz-Institute for Primate Research, Göttingen, Germany.ORCID 0000-0001-9408-3131

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HLA-E expression plays a central role for modulation of NK cell function by interaction with inhibitory NKG2A and stimulatory NKG2C receptors on canonical and adaptive NK cells, respectively. Here, we demonstrate that infection of human primary lung tissue with SARS-CoV-2 leads to increased HLA-E expression and show that processing of the peptide YLQPRTFLL from the spike protein is primarily responsible for the strong, dose-dependent increase of HLA-E. Targeting the peptide site within the spike protein revealed that a single point mutation was sufficient to abrogate the increase in HLA-E expression. Spike-mediated induction of HLA-E differentially affected NK cell function: whereas degranulation, IFN-γ production, and target cell cytotoxicity were enhanced in NKG2C

Indexed as

COVID-19Histocompatibility Antigens Class IHLA-E AntigensKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily CSARS-CoV-2Spike Glycoprotein, CoronavirusAdaptive ImmunityFemaleHumansLungMaleMiddle AgedHistocompatibility Antigens Class IHLA-E AntigensKLRC1 protein, humanKLRC2 protein, humanNK Cell Lectin-Like Receptor Subfamily CSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2adaptive NK cellsHLAENKG2ANKG2CSARS-CoV-2 infection

Identifiers

PMID38804979
PMCPMC11212573

What OpenQuestion holds

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LicenceCC BY
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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.