Observational studyGut2014
The paradox of NKp46+ natural killer cells: drivers of severe hepatitis C virus-induced pathology but in-vivo resistance to interferon α treatment.
Observational study in Gut, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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.
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.
Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Interferon Alpha Induces Sustained Changes in NK Cell Responsiveness to Hepatitis B Viral Load Suppression In Vivo.PLoS pathogens · 2016Trial
- Evaluation of the HBV liver reservoir with fine needle aspirates.JHEP reports : innovation in hepatology · 2023Article
- Immunological Monitoring in Hepatitis C Virus Controlled Human Infection Model.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023Article
- Assessing immunological and virological responses in the liver: Implications for the cure of chronic hepatitis B virus infection.JHEP reports : innovation in hepatology · 2022Review
- Review article: emerging insights into the immunopathology, clinical and therapeutic aspects of hepatitis delta virus.Alimentary pharmacology & therapeutics · 2022Review
- Decreased CD57 expression of natural killer cells enhanced cytotoxicity in patients with primary sclerosing cholangitis.Frontiers in immunology · 2022Article
- Hepatitis C Virus Relapse After Ultrashort Direct-Acting Antiviral Therapy Associates With Expression of Genes Involved With Natural Killer-Cell and CD8Open forum infectious diseases · 2021Article
- Diversity Outbred Mice Reveal the Quantitative Trait Locus and Regulatory Cells of HER2 Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Immunomodulation of the Natural Killer Cell Phenotype and Response during HCV Infection.Journal of clinical medicine · 2020Review
- Rituximab depletion of intrahepatic B cells to control refractory hepatic autoimmune overlap syndrome.QJM : monthly journal of the Association of Physicians · 2019Article
- Liver cirrhosis in HIV/HCV-coinfected individuals is related to NK cell dysfunction and exhaustion, but not to an impaired NK cell modulation by CD4Journal of the International AIDS Society · 2019Article
- Article
- CEACAM1 Is Associated With the Suppression of Natural Killer Cell Function in Patients With Chronic Hepatitis C.Hepatology communications · 2018Article
- Review
- IL-12 and IL-15 induce the expression of CXCR6 and CD49a on peripheral natural killer cells.Immunity, inflammation and disease · 2018Article
- Current progress in host innate and adaptive immunity against hepatitis C virus infection.Hepatology international · 2017Review
- Non-neutralizing epitopes induce robust hepatitis C virus (HCV)-specific antibody-dependent CD56Clinical and experimental immunology · 2017Article
- Review
- Article
- Hepatitis C Virus and Human Cytomegalovirus-Natural Killer Cell Subsets in Persistent Viral Infections.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveThere is evidence that natural killer (NK) cells help control persistent viral infections including hepatitis C virus (HCV). The phenotype and function of blood and intrahepatic NK cells, in steady state and after interferon (IFN) α treatment has not been fully elucidated.
designWe performed a comparison of NK cells derived from blood and intrahepatic compartments in multiple paired samples from patients with a variety of chronic liver diseases. Furthermore, we obtained serial paired samples from an average of five time points in HCV patients treated with IFNα.
resultsLiver NK cells demonstrate a distinct activated phenotype compared to blood manifested as downregulation of the NK cell activation receptors CD16, NKG2D, and NKp30; with increased spontaneous degranulation and IFN production. In contrast, NKp46 expression was not downregulated. Indeed, NKp46-rich NK populations were the most activated, correlating closely with the severity of liver inflammation. Following initiation of IFNα treatment there was a significant increase in the proportion of intrahepatic NK cells at days 1 and 3. NKp46-rich NK populations demonstrated no reserve activation capacity with IFNα treatment and were associated with poor viral control on treatment and treatment failure.
conclusionsNKp46 marks out pathologically activated NK cells, which may result from a loss of homeostatic control of activating receptor expression in HCV. Paradoxically these pathological NK cells do not appear to be involved in viral control in IFNα-treated individuals and, indeed, predict slower rates of viral clearance.
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What OpenQuestion holds
Registered trials
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.