Evidence map›Paper›PMID 29026144›Full record

ArticleScientific reports2017

Increased NK cell immunity in a transgenic mouse model of NKp46 overexpression.

Ariella Glasner, Batya Isaacson, Sergey Viukov, Tzahi Neuman, Nehemya Friedman, Michal Mandelboim, Veronika Sexl, Jacob H Hanna, Ofer Mandelboim

Expression of concernOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  6. Review
  7. NK Cells in aFrontiers in immunology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 2 countries.

Ariella GlasnerThe Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem, Israel.
Batya IsaacsonThe Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem, Israel.
Sergey ViukovDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, 7610001, Israel.
Tzahi NeumanDepartment of Pathology, Hadassah Medical Organization, The Hebrew University Medical Center, Jerusalem, Israel.
Nehemya FriedmanCentral Virology Laboratory, Ministry of Health, Chaim Sheba Medical Center, Tel-Hashomer, Ramat-Gan, Israel.
Michal MandelboimCentral Virology Laboratory, Ministry of Health, Chaim Sheba Medical Center, Tel-Hashomer, Ramat-Gan, Israel.
Veronika SexlInstitute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria.
Jacob H HannaDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, 7610001, Israel.ORCID 0000-0003-2042-9974
Ofer MandelboimThe Lautenberg Center for General and Tumor Immunology, Department of Immunology and Cancer Research, IMRIC, Faculty of Medicine, The Hebrew University Medical School, Jerusalem, Israel. oferm@ekmd.huji.ac.il.
Hebrew University of Jerusalem · ILTel Aviv University · ILWeizmann Institute of Science · ILHadassah Medical Center · ILUniversity of Veterinary Medicine Vienna · AT

Funding

European Research Council 320473
6 · The paper itself

Abstract

Natural Killer (NK) cells employ activating receptors like the Natural Cytotoxicity Receptors (NCRs: NKp30, NKp44 and NKp46), of which only NKp46 has a mouse orthologue (Ncr1), to eliminate abnormal cells. NKp46/Ncr1 is considered a selective marker for NK cells, although it is also found on a subset of ILCs, where it appears to be without function. The influenza virus hemagglutinin (HA) was the first ligand identified for Ncr1/NKp46 followed by other viral, bacterial and even fungal ligands. NKp46/Ncr1 also recognizes unknown self and tumor ligands. Here we describe the generation of a transgenic mouse where the Ncr1 gene is expressed in the Rosa locus, preceded by a floxed stop sequence allowing Ncr1/NKp46 expression in various tissues upon crossing with Cre transgenic mouse lines. Surprisingly, while several crossings were attempted, Ncr1 overexpression was successful only where cre recombinase expression was dependent on the Ncr1 promoter. Ncr1 overexpression in NK cells increased NK cell immunity in two hallmark Ncr1 related pathologies, influenza virus infection and B16 melanoma. These data suggest that increasing NK cell cytotoxicity by enforced NKp46/Ncr1 expression serves as a potential therapeutic opportunity for the treatment of various pathologies, and in immunotherapy.

Indexed as

AnimalsAntigens, LyDisease Models, AnimalHumansInfluenza, HumanKiller Cells, NaturalMelanoma, ExperimentalMiceMice, TransgenicNatural Cytotoxicity Triggering Receptor 1OrthomyxoviridaeAntigens, LyNatural Cytotoxicity Triggering Receptor 1Ncr1 protein, mouse

Identifiers

PMID29026144
PMCPMC5638832
OpenAlexW2764109170

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.