Evidence map›Paper›PMID 21937646›Full record

ArticleJournal of virology2011

Cell-to-cell contact with hepatitis C virus-infected cells reduces functional capacity of natural killer cells.

Joo Chun Yoon, Jong-Baeck Lim, Jeon Han Park, Jae Myun Lee

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Roseoside Is a Bioactive Compound inMolecules (Basel, Switzerland) · 2024
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Natural killer cells in antiviral immunity.Nature reviews. Immunology · 2022
    Review
  8. Article
  9. Control of HCV Infection by Natural Killer Cells and Macrophages.Cold Spring Harbor perspectives in medicine · 2020
    Review
  10. Review
  11. NK Cell Hyporesponsiveness: More Is Not Always Better.International journal of molecular sciences · 2019
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Hepatitis C virus: life cycle in cells, infection and host response, and analysis of molecular markers influencing the outcome of infection and response to therapy.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2016
    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

4 authors at 1 institution in 1 country.

Joo Chun YoonDepartment of Microbiology, Yonsei University College of Medicine, 250 Seongsanno, Seodaemun-gu, Seoul 120-752, Republic of Korea.
Jong-Baeck Lim
Jeon Han Park
Jae Myun Lee
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The distinct feature of hepatitis C virus (HCV) infection is a high incidence of chronicity. The reason for chronic HCV infection has been actively investigated, and impairment of innate and adaptive immune responses against HCV is proposed as a plausible cause. Whereas functional impairment of HCV-specific T cells is well characterized, the role and functional status of natural killer (NK) cells in each phase of HCV infection are still elusive. We therefore investigated whether direct interaction between NK cells and HCV-infected cells modulates NK cell function. HCV-permissive human hepatoma cell lines were infected with cell culture-generated HCV virions and cocultured with primary human NK cells. Cell-to-cell contact between NK cells and HCV-infected cells reduced NK cells' capacity to degranulate and lyse target cells, especially in the CD56(dim) NK cell subset, which is characterized by low-density surface expression of CD56. The decrease in degranulation capacity was correlated with downregulated expression of NK cell-activating receptors, such as NKG2D and NKp30, on NK cells. The ability of NK cells to produce and secrete gamma interferon (IFN-γ) also diminished after exposure to HCV-infected cells. The decline of IFN-γ production was consistent with the reduction of NK cell degranulation. In conclusion, cell-to-cell contact with HCV-infected cells negatively modulated functional capacity of NK cells, and the inhibition of NK cell function was associated with downregulation of NK-activating receptors on NK cell surfaces. These observations suggest that direct cell-to-cell interaction between NK cells and HCV-infected hepatocytes may impair NK cell function in vivo and thereby contribute to the establishment of chronic infection.

Indexed as

Cell CommunicationCarcinoma, HepatocellularCells, CulturedCytotoxicity, ImmunologicFlow CytometryHepacivirusHepatitis C, ChronicHepatocytesHumansInterferon-gammaKiller Cells, NaturalLiver NeoplasmsLymphocyte ActivationNatural Cytotoxicity Triggering Receptor 3NK Cell Lectin-Like Receptor Subfamily KT-LymphocytesInterferon-gammaKLRK1 protein, humanNatural Cytotoxicity Triggering Receptor 3NCR3 protein, humanNK Cell Lectin-Like Receptor Subfamily K

Identifiers

PMID21937646
PMCPMC3209413
OpenAlexW2131615567

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.