Evidence map›Paper›PMID 21901096›Full record

ArticlePLoS pathogens2011

Modulation of NKp30- and NKp46-mediated natural killer cell responses by poxviral hemagglutinin.

Mostafa Jarahian, Manuela Fiedler, André Cohnen, Dominik Djandji, Günter J Hämmerling, Cornelius Gati, Adelheid Cerwenka, Peter C Turner, Richard W Moyer, Carsten Watzl and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 112 citations in OpenAlex.

  1. NKp30: A Key Membrane Molecule in the Fight Against Cancer and Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Human natural killer cells: Form, function, and development.The Journal of allergy and clinical immunology · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

12 authors at 5 institutions in 2 countries.

Mostafa JarahianTranslational Immunology Research Unit, German Cancer Research Center, Heidelberg, Germany.
Manuela Fiedler
André Cohnen
Dominik Djandji
Günter J Hämmerling
Cornelius Gati
Adelheid Cerwenka
Peter C Turner
Richard W Moyer
Carsten Watzl
Hartmut Hengel
Frank Momburg
Heidelberg University · DEHeinrich Heine University Düsseldorf · DEFlorida College · USGerman Cancer Research Center · DEUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK) cells are an important element in the immune defense against the orthopox family members vaccinia virus (VV) and ectromelia virus (ECTV). NK cells are regulated through inhibitory and activating signaling receptors, the latter involving NKG2D and the natural cytotoxicity receptors (NCR), NKp46, NKp44 and NKp30. Here we report that VV infection results in an upregulation of ligand structures for NKp30 and NKp46 on infected cells, whereas the binding of NKp44 and NKG2D was not significantly affected. Likewise, infection with ectromelia virus (ECTV), the mousepox agent, enhanced binding of NKp30 and, to a lesser extent, NKp46. The hemagglutinin (HA) molecules from VV and ECTV, which are known virulence factors, were identified as novel ligands for NKp30 and NKp46. Using NK cells with selectively silenced NCR expression and NCR-CD3ζ reporter cells, we observed that HA present on the surface of VV-infected cells, or in the form of recombinant soluble protein, was able to block NKp30-triggered activation, whereas it stimulated the activation through NKp46. The net effect of this complex influence on NK cell activity resulted in a decreased NK lysis susceptibility of infected cells at late time points of VV infection when HA was expression was pronounced. We conclude that poxviral HA represents a conserved ligand of NCR, exerting a novel immune escape mechanism through its blocking effect on NKp30-mediated activation at a late stage of infection.

Indexed as

AnimalsCell LineEctromelia virusGene Expression Regulation, ViralHemagglutininsHumansKiller Cells, NaturalMiceNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 3PlasmidsRecombinant Fusion ProteinsRNA, Small InterferingUp-RegulationVaccinia virusHemagglutininsNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 3NCR1 protein, humanNCR3 protein, humanRecombinant Fusion ProteinsRNA, Small Interfering

Identifiers

PMID21901096
PMCPMC3161980
OpenAlexW1992692237

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.