Evidence map›Paper›PMID 16322112›Full record

ArticleGut2006

Surface expression and cytolytic function of natural killer cell receptors is altered in chronic hepatitis C.

J Nattermann, G Feldmann, G Ahlenstiel, B Langhans, T Sauerbruch, U Spengler

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

129 citing papers in PubMed, 231 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Long-term effect on natural killer cells by interferon-α therapy on the outcomes of HCV infection.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Trial
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Innate immunity and early liver inflammation.Frontiers in immunology · 2023
    Review
  11. Article
  12. The antifibrotic role of natural killer cells in liver fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
  13. Review
  14. Review
  15. Natural killer cells in antiviral immunity.Nature reviews. Immunology · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Role of NKG2a/ciScience · 2021
    Article
  20. Review

69 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

6 authors at 1 institution in 1 country.

J NattermannDepartment of Internal Medicine I, Rheinische Friedrich-Wilhelms-Universitaet, Germany. Jacob.Nattermann@ukb.uni-bonn.de
G Feldmann
G Ahlenstiel
B Langhans
T Sauerbruch
U Spengler
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionImpaired activity of natural killer (NK) cells has been proposed as a mechanism contributing to viral persistence in hepatitis C virus (HCV) infection. As the function of NK cells is primarily regulated by NK cell receptors (NKR), we analysed whether decreased NK cell function in hepatitis C may be related to dysregulated NKR expression. PATIENTS AND

methodsExpression of NK cell was analysed by flow cytometry on lymphocytes from HCV(+) subjects (n = 30), patients who became HCV(-) after antiviral therapy (n = 10), healthy individuals (n = 10), and hepatitis B virus (HBV) infected patients (n = 9). Cytolytic function of lymphocytes was studied in a redirected lysis assay and in a standard 51chromium release cytotoxicity assay, respectively.

resultsIn patients with chronic hepatitis C, we found a significantly reduced proportion of NKp46 and NKp30 expressing NK cells compared with healthy and HBV infected subjects. Low expression of natural cytotoxicity receptor (NCR) was also confirmed in in vitro activated NK cell populations derived from HCV patients compared with uninfected donors. In contrast, patients who cleared HCV under antiviral therapy showed normal expression of NKp44, NKp30, and NKp46. Reduced NCR expression in chronic hepatitis C was associated with a parallel decrease in NCR mediated target cell killing. Furthermore, we found a significantly increased proportion of NKG2A expressing NK cells and CD8+ T cells in HCV positive patients, resulting in a reduced cytolytic activity against cells incubated with the HLA-E stabilising peptide HCV core35-44.

conclusionThe present study indicates that defective expression of NKR represents a novel mechanism contributing to impaired function of NK cells and CD8+ T cells in chronic hepatitis C.

Indexed as

AdultAgedAntiviral AgentsCD8-Positive T-LymphocytesCells, CulturedCytotoxicity, ImmunologicFemaleHepatitis C, ChronicHumansImmune ToleranceKiller Cells, NaturalMaleMembrane GlycoproteinsMiddle AgedNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 2Antiviral AgentsMembrane GlycoproteinsNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 2Natural Cytotoxicity Triggering Receptor 3NCR1 protein, humanNCR2 protein, humanNCR3 protein, humanReceptors, Immunologic

Identifiers

PMID16322112
PMCPMC1856237
OpenAlexW2153765164

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.