Evidence map›Paper›PMID 27583440›Full record

ArticlePloS one2016

IL-28B Genetic Variants Determine the Extent of Monocyte-Induced Activation of NK Cells in Hepatitis C.

Benjamin Krämer, Claudia Finnemann, Beatriz Sastre, Philipp Lutz, Andreas Glässner, Franziska Wolter, Felix Goeser, Pavlos Kokordelis, Dominik Kaczmarek, Hans-Dieter Nischalke and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Trial
  2. Review
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

13 authors at 2 institutions in 2 countries.

Benjamin KrämerDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.ORCID http://orcid.org/0000-0002-1385-9709
Claudia FinnemannDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Beatriz SastreDepartment of Infectious Diseases, Institute for Health Research (IRYCIS), University Hospital Ramón y Cajal, Madrid, Spain.
Philipp LutzDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Andreas GlässnerDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Franziska WolterDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Felix GoeserDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Pavlos KokordelisDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Dominik KaczmarekDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Hans-Dieter NischalkeDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Christian P StrassburgDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Ulrich SpenglerDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
Jacob NattermannDepartment of Internal Medicine I, University of Bonn, Bonn, Germany.
University of Bonn · DEInstituto Cajal · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmuno-genetic studies suggest a functional link between NK cells and λ-IFNs. We recently showed that NK cells are negative for the IFN-λ receptor IFN-λR1 and do not respond to IFN-λ, suggesting a rather indirect association between IL-28B genotype and NK cell activity.

methodsA total of 75 HCV(+) patients and 67 healthy controls were enrolled into this study. IL-28B (rs12979860) and IFNL-4 (rs368234815) genotypes were determined by rtPCR. Total PBMC, monocytes, and NK cells were stimulated with IL-29, the TLR-7/8 agonist R848, or a combination of both. NK cell IFN-γ response was analysed by FACS. IL-12 and IL-18 secretion of monocytes was studied by ELISA. In blocking experiments anti-IL-12/anti-IL-18 were used.

resultsFollowing stimulation of total PBMCs with R848 we found NK cell IFN- γ responses to vary with the IL-28B genotype, with carriers of a T/T genotype displaying the lowest frequency of IFN-γ(+)NK cells. When isolated NK cells were studied no such associations were observed, indicating an indirect association between IL-28B genotype and NK cell activity. Accordingly, we found R848-stimulated monocytes of patients with a T/T genotype to be significantly less effective in triggering NK cell IFN- γ production than monocytes from carriers of a non-T/T genotype. In line with these findings we observed monocytes from T/T patients to secrete significantly lower concentrations of IL-12 than monocytes from non-T/T individuals.

conclusionsOur data indicate that monocytes from carriers of an IL-28B T/T genotype display a reduced ability to stimulate NK cell activity and, thus, provide a link between IL-28B genotype and NK functions.

Indexed as

Genetic VariationFemaleGenotypeHepatitis CHumansInterferon LambdaInterferonsInterleukin-12InterleukinsKiller Cells, NaturalLymphocyte ActivationMaleMiddle AgedMonocytesInterferon Lambdainterferon-lambda, humanInterferonsInterleukin-12Interleukins

Identifiers

PMID27583440
PMCPMC5008784
OpenAlexW2517584841

What OpenQuestion holds

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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.