Evidence map›Paper›PMID 27116381›Full record

ArticleJournal of innate immunity2016

Cytomegalovirus-Infected Primary Endothelial Cells Trigger NKG2C+ Natural Killer Cells.

Zakia Djaoud, Raphaëlle Riou, Pierre-Jean Gavlovsky, Souad Mehlal, Céline Bressollette, Nathalie Gérard, Katia Gagne, Béatrice Charreau, Christelle Retière

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Impact of Methylated Cyclodextrin KLEPTOSEInternational journal of molecular sciences · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. NK cells in host responses to viral infections.Current opinion in immunology · 2017
    Review
  13. Review
  14. Expansions of Cytotoxic CD4Frontiers in immunology · 2017
    Review
  15. Review
  16. Review
  17. 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

9 authors at 4 institutions in 1 country.

Zakia DjaoudEtablissement Franx00E7;ais du Sang, ImmunoVirologie et Polymorphisme Gx00E9;nx00E9;tique, Universitx00E9; de Nantes, Nantes, France.
Raphaëlle Riou
Pierre-Jean Gavlovsky
Souad Mehlal
Céline Bressollette
Nathalie Gérard
Katia Gagne
Béatrice Charreau
Christelle Retière
Établissement Français du Sang · FRCenter for Research in Transplantation and Translational ImmunologyNantes Université · FRCentre Hospitalier Universitaire de Nantes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among innate cells, natural killer (NK) cells play a crucial role in the defense against cytomegalovirus (CMV). In some individuals, CMV infection induces the expansion of NKG2C+ NK cells that persist after control of the infection. We have previously shown that KIR2DL+ NK cells, in contrast to NKG2C+ NK cells, contribute to controlling CMV infection using a CMV-infected monocyte-derived dendritic cell (MDDC) model. However, the nature of CMV-infected cells contributing to the expansion of the NKG2C+ NK cell subset remains unclear. To gain more insight into this question, we investigated the contribution of NKG2C+ NK cell activation by CMV-infected primary human aortic endothelial cells (EC) isolated from kidney transplant donors, which constitutively express the human leukocyte antigen (HLA)-E molecule. Here, we show that, although classic HLA class I expression was drastically downregulated, nonclassic HLA-E expression was maintained in CMV-infected EC. By comparing HLA expression patterns in CMV-infected EC, fibroblasts and MDDC, we demonstrate a cell-dependent modulation of HLA-E expression by CMV infection. NKG2C+ NK cell degranulation was significantly triggered by CMV-infected EC regardless of the nature of the HLA-E allele product. EC, predominantly present in vessels, may constitute a privileged site for CMV infection that drives a 'memory' NKG2C+ NK cell subset.

Indexed as

AortaCell DegranulationCell ProliferationCells, CulturedCytomegalovirusCytomegalovirus InfectionsDendritic CellsEndothelium, VascularFibroblastsHistocompatibility Antigens Class IHLA-E AntigensHumansImmunologic MemoryKiller Cells, NaturalLymphocyte ActivationLymphocyte SubsetsHistocompatibility Antigens Class IHLA-E AntigensKIR2DL1 protein, humanKLRC2 protein, humanNK Cell Lectin-Like Receptor Subfamily CReceptors, KIR2DL1

Identifiers

PMID27116381
PMCPMC6738823
OpenAlexW2342670006

What OpenQuestion 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 OpenQuestion graph.