Evidence map›Paper›PMID 26094914›Full record

ArticleImmunology2015

NKp30 isoforms in patients with chronic hepatitis C virus infection.

Stefania Mantovani, Dalila Mele, Barbara Oliviero, Giorgio Barbarini, Stefania Varchetta, Mario U Mondelli

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. NKp30: A Key Membrane Molecule in the Fight Against Cancer and Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Human NK Cells Lyse Th2-Polarizing Dendritic Cells via NKp30 and DNAM-1.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Natural Killer Cells and Liver Fibrosis.Frontiers in immunology · 2016
    Review
  16. Article
  17. Article
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 2 institutions in 1 country.

Stefania MantovaniResearch Laboratories, Department of Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Dalila MeleResearch Laboratories, Department of Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Barbara OlivieroResearch Laboratories, Department of Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Giorgio BarbariniDivision of Tropical Medicine, Department of Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Stefania VarchettaResearch Laboratories, Department of Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Mario U MondelliResearch Laboratories, Department of Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Istituti di Ricovero e Cura a Carattere Scientifico · ITPoliclinico San Matteo Fondazione · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK) cells play an important role in virus infection, their action being regulated by several activating and inhibitory receptors. The NKp30 activating receptor and its isoforms have recently emerged as important determinants of efficient NK cell responses. We determined the relative proportions of NKp30 isoforms in patients with chronic hepatitis C virus (HCV) infection and healthy donors (HD). NK cell function (degranulation and cytokine production) and correlations with clinical parameters were assessed following unsupervised hierarchical clustering of patients according to isoform expression. NKp30 receptor expression on NK cells and all isoforms were reduced in HCV-infected patients. Patients were clustered into two groups: the HCV-1 group had similar isoform expression to the HD group, whereas the HCV-2 group had lower expression. The latter showed a better functional activity, and a higher proportion of the activating a isoform and of the NKp30 isoform a/c ratio compared with the HCV-1 cluster. There was a positive correlation between the activating a isoform and liver stiffness and an inverse relationship between the immunosuppressive c isoform and the fibrosis 4 score, suggesting a potentially important role of NKp30 isoforms in influencing liver damage and ensuing fibrosis.

Indexed as

AdultAgedAged, 80 and overCase-Control StudiesCell DegranulationCell LineCluster AnalysisCoculture TechniquesCytokinesDisease ProgressionFemaleGenotypeHepacivirusHepatitis C, ChronicHost-Pathogen InteractionsHumansCytokinesNatural Cytotoxicity Triggering Receptor 3NCR3 protein, humanProtein Isoformsinterferon-γliver fibrosisnatural killer cellsunsupervised hierarchical clustering

Identifiers

PMID26094914
PMCPMC4582964
OpenAlexW1512900631

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.