Evidence map›Paper›PMID 25329659›Full record

ArticlePLoS pathogens2014

Human cytomegalovirus drives epigenetic imprinting of the IFNG locus in NKG2Chi natural killer cells.

Merlin Luetke-Eversloh, Quirin Hammer, Pawel Durek, Karl Nordström, Gilles Gasparoni, Matthias Pink, Alf Hamann, Jörn Walter, Hyun-Dong Chang, Jun Dong and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

165 citing papers in PubMed, 1 synthesis or guideline pooled it, 250 citations in OpenAlex.

  1. Pooled it
  2. NK Cell Activity and CD57Frontiers in immunology · 2020
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  6. HLA-E-Directed Accumulation of KIRInternational journal of molecular sciences · 2026
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105 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

11 authors at 2 institutions in 1 country.

Merlin Luetke-EverslohInnate Immunity, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Quirin HammerInnate Immunity, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Pawel DurekExperimental Rheumatology, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany; Cell Biology, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Karl NordströmDepartment of Genetics, University of Saarland, Saarbrücken, Germany.
Gilles GasparoniDepartment of Genetics, University of Saarland, Saarbrücken, Germany.
Matthias PinkExperimental Rheumatology, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Alf HamannExperimental Rheumatology, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Jörn WalterDepartment of Genetics, University of Saarland, Saarbrücken, Germany.
Hyun-Dong ChangCell Biology, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Jun DongCell Biology, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
Chiara RomagnaniInnate Immunity, Deutsches Rheuma-Forschungszentrum - A Leibniz Institute, Berlin, Germany.
German Rheumatism Research Centre · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Memory type 1 T helper (T(H)1) cells are characterized by the stable expression of interferon (IFN)-γ as well as by the epigenetic imprinting of the IFNG locus. Among innate cells, NK cells play a crucial role in the defense against cytomegalovirus (CMV) and represent the main source of IFN-γ. Recently, it was shown that memory-like features can be observed in NK cell subsets after CMV infection. However, the molecular mechanisms underlying NK cell adaptive properties have not been completely defined. In the present study, we demonstrated that only NKG2Chi NK cells expanded in human CMV (HCMV) seropositive individuals underwent epigenetic remodeling of the IFNG conserved non-coding sequence (CNS) 1, similar to memory CD8(+) T cells or T(H)1 cells. The accessibility of the CNS1 was required to enhance IFN-γ transcriptional activity in response to NKG2C and 2B4 engagement, which led to consistent IFN-γ production in NKG2C(hi) NK cells. Thus, our data identify epigenetic imprinting of the IFNG locus as selective hallmark and crucial mechanism driving strong and stable IFN-γ expression in HCMV-specific NK cell expansions, providing a molecular basis for the regulation of adaptive features in innate cells.

Indexed as

Epigenesis, GeneticCD56 AntigenCD8-Positive T-LymphocytesCell DifferentiationCytomegalovirusCytomegalovirus InfectionsGenetic LociHumansInterferon-gammaKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily CCD56 AntigenInterferon-gammaKLRC2 protein, humanNK Cell Lectin-Like Receptor Subfamily C

Identifiers

PMID25329659
PMCPMC4199780
OpenAlexW2002718676

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.