Evidence map›Paper›PMID 23592985›Full record

ArticlePLoS pathogens2013

Human cytomegalovirus infection elicits new decidual natural killer cell effector functions.

Johan Siewiera, Hicham El Costa, Julie Tabiasco, Alain Berrebi, Géraldine Cartron, Philippe Le Bouteiller, Philippe Bouteiller, Nabila Jabrane-Ferrat

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

105 citing papers in PubMed, 158 citations in OpenAlex.

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  12. Immune surveillance of cytomegalovirus in tissues.Cellular & molecular immunology · 2024
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45 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
    Bouteiller, Philippe [corrected to Le Bouteiller, Philippe]
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 3 countries.

Johan SiewieraInstitut National de la Santé et de la Recherche Médicale, UMR 1043, Toulouse, France.
Hicham El Costa
Julie Tabiasco
Alain Berrebi
Géraldine Cartron
Philippe Le Bouteiller
Philippe Bouteiller
Nabila Jabrane-Ferrat
Université Toulouse III - Paul Sabatier · FRHôpital Paule de Viguier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the first trimester of pregnancy the uterus is massively infiltrated by decidual natural killer cells (dNK). These cells are not killers, but they rather provide a microenvironment that is propitious to healthy placentation. Human cytomegalovirus (HCMV) is the most common cause of intrauterine viral infections and a known cause of severe birth defects or fetal death. The rate of HCMV congenital infection is often low in the first trimester of pregnancy. The mechanisms controlling HCMV spreading during pregnancy are not yet fully revealed, but evidence indicating that the innate immune system plays a role in controlling HCMV infection in healthy adults exists. In this study, we investigated whether dNK cells could be involved in controlling viral spreading and in protecting the fetus against congenital HCMV infection. We found that freshly isolated dNK cells acquire major functional and phenotypic changes when they are exposed to HCMV-infected decidual autologous fibroblasts. Functional studies revealed that dNK cells, which are mainly cytokines and chemokines producers during normal pregnancy, become cytotoxic effectors upon their exposure to HCMV-infected autologous decidual fibroblasts. Both the NKG2D and the CD94/NKG2C or 2E activating receptors are involved in the acquired cytotoxic function. Moreover, we demonstrate that CD56(pos) dNK cells are able to infiltrate HCMV-infected trophoblast organ culture ex-vivo and to co-localize with infected cells in situ in HCMV-infected placenta. Taken together, our results present the first evidence suggesting the involvement of dNK cells in controlling HCMV intrauterine infection and provide insights into the mechanisms through which these cells may operate to limit the spreading of viral infection to fetal tissues.

Indexed as

CD56 AntigenCell LineCytomegalovirusCytomegalovirus InfectionsDeciduaFas Ligand ProteinFemaleHEK293 CellsHumansKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DNK Cell Lectin-Like Receptor Subfamily KPlacentationPregnancyPregnancy Trimester, FirstCD56 AntigenFASLG protein, humanFas Ligand ProteinKLRC2 protein, humanKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DNK Cell Lectin-Like Receptor Subfamily KTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID23592985
PMCPMC3617138
OpenAlexW2112988638

What OpenQuestion holds

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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.