Evidence map›Paper›PMID 34773897›Full record

ArticleCellular immunology2022

SARS-CoV-2 peptides bind to NKG2D and increase NK cell activity.

Hanna Kim, Jae-Eun Byun, Suk Ran Yoon, Hashem Koohy, Haiyoung Jung, Inpyo Choi

Open access · hybridAbstract read
In one paragraph

Article in Cellular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. SARS-CoV-2 infection impairs NK cell functionsFrontiers in immunology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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

6 authors at 3 institutions in 2 countries.

Hanna KimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Jae-Eun ByunImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea; Department of Biochemistry, School of Life Sciences, Chungbuk National University, Cheongju, Republic of Korea.
Suk Ran YoonImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea; Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea.
Hashem KoohyMRC Human Immunology Unit, Medical Research Council (MRC) Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine (WIMM), John Radcliffe Hospital, University of Oxford, Oxford, UK. Electronic address: hashem.koohy@rdm.ox.ac.uk.
Haiyoung JungImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea; Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea. Electronic address: haiyoung@kribb.re.kr.
Inpyo ChoiImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea; Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea. Electronic address: ipchoi@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KRJohn Radcliffe Hospital · GBKorea University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune dysregulation is commonly observed in patients with coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces severe lung inflammation and innate immune cell dysregulation. However, the precise interaction between SARS-CoV-2 and the innate immune system is currently unknown. To understand the interaction between SARS-CoV-2 and natural killer (NK) cells, several SARS-CoV-2 S protein peptides capable of binding to the NKG2D receptor were screened by in silico analysis. Among them, two peptides, cov1 and cov2, bound to NK cells and NKG2D receptors. These cov peptides increased NK cytotoxicity toward lung cancer cells, stimulated interferon gamma (IFN-γ) production by NK cells, and likely mediated these responses through the phosphorylation of Vav1, a key downstream-signaling molecule of NKG2D and NK activation genes. The direct interaction between SARS-CoV-2 and NK cells is a novel finding, and modulation of this interaction has potential clinical application as a therapeutic target for COVID-19.

Indexed as

Amino Acid SequenceCell Line, TumorCOVID-19Cytotoxicity, ImmunologicHumansInterferon-gammaKiller Cells, NaturalLungLymphocyte ActivationNK Cell Lectin-Like Receptor Subfamily KPeptidesProtein BindingSARS-CoV-2Signal TransductionSpike Glycoprotein, CoronavirusInterferon-gammaNK Cell Lectin-Like Receptor Subfamily KPeptidesSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2CytotoxicityIFN-γNKNKG2DPeptideSARS-Cov-2

Identifiers

PMID34773897
PMCPMC8577527
OpenAlexW3212607594

What Socratic holds

Textmetadata
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 Socratic graph.