Evidence map›Paper›PMID 22316211›Full record

ArticleBMC immunology2012

Cervical cancer cell lines expressing NKG2D-ligands are able to down-modulate the NKG2D receptor on NKL cells with functional implications.

Miriam I Jimenez-Perez, Luis F Jave-Suarez, Pablo C Ortiz-Lazareno, Alejandro Bravo-Cuellar, Oscar Gonzalez-Ramella, Adriana Aguilar-Lemarroy, Georgina Hernandez-Flores, Ana L Pereira-Suarez, Adrian Daneri-Navarro, Susana del Toro-Arreola

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Activities of stromal and immune cells in HPV-related cancers.Journal of experimental & clinical cancer research : CR · 2018
    Review
  8. Article
  9. Article
  10. Anti-NKG2D mAb: A New Treatment for Crohn's Disease?International journal of molecular sciences · 2017
    Review
  11. Article
  12. hrHPV E5 oncoprotein: immune evasion and related immunotherapies.Journal of experimental & clinical cancer research : CR · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

10 authors at 2 institutions in 1 country.

Miriam I Jimenez-PerezDepartamento de Fisiología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico.
Luis F Jave-Suarez
Pablo C Ortiz-Lazareno
Alejandro Bravo-Cuellar
Oscar Gonzalez-Ramella
Adriana Aguilar-Lemarroy
Georgina Hernandez-Flores
Ana L Pereira-Suarez
Adrian Daneri-Navarro
Susana del Toro-Arreola
Universidad de Guadalajara · MXMexican Social Security Institute · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical cancer represents the third most commonly diagnosed cancer and the fourth leading cause of cancer-related deaths in women worldwide. Natural killer (NK) cells play an important role in the defense against viruses, intracellular bacteria and tumors. NKG2D, an activating receptor on NK cells, recognizes MHC class I chain-related molecules, such as MICA/B and members of the ULBP/RAET1 family. Tumor-derived soluble NKG2D-ligands have been shown to down-modulate the expression of NKG2D on NK cells. In addition to the down-modulation induced by soluble NKG2D-ligands, it has recently been described that persistent cell-cell contact can also down-modulate NKG2D expression. The goal of this study was to determine whether the NKG2D receptor is down-modulated by cell-cell contact with cervical cancer cells and whether this down-modulation might be associated with changes in NK cell activity.

resultsWe demonstrate that NKG2D expressed on NKL cells is down-modulated by direct cell contact with cervical cancer cell lines HeLa, SiHa, and C33A, but not with non-tumorigenic keratinocytes (HaCaT). Moreover, this down-modulation had functional implications. We found expression of NKG2D-ligands in all cervical cancer cell lines, but the patterns of ligand distribution were different in each cell line. Cervical cancer cell lines co-cultured with NKL cells or fresh NK cells induced a marked diminution of NKG2D expression on NKL cells. Additionally, the cytotoxic activity of NKL cells against K562 targets was compromised after co-culture with HeLa and SiHa cells, while co-culture with C33A increased the cytotoxic activity of the NKL cells.

conclusionsOur results suggest that differential expression of NKG2D-ligands in cervical cancer cell lines might be associated with the down-modulation of NKG2D, as well as with changes in the cytotoxic activity of NKL cells after cell-cell contact with the tumor cells.

Indexed as

CarcinomaCarrier ProteinsCell CommunicationCytotoxicity, ImmunologicDown-RegulationFemaleGene Expression Regulation, NeoplasticGPI-Linked ProteinsHeLa CellsHistocompatibility Antigens Class IHumansIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsKiller Cells, NaturalLigandsMembrane ProteinsCarrier ProteinsGPI-Linked ProteinsHistocompatibility Antigens Class IIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsLigandsMembrane ProteinsNK Cell Lectin-Like Receptor Subfamily KRAET1E protein, humanULBP1 protein, humanULBP2 protein, humanULBP3 protein, human

Identifiers

PMID22316211
PMCPMC3364150
OpenAlexW2059102679

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LicenceCC BY
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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.