ArticleJournal of clinical immunology2010
Impairment of TLR7-dependent signaling in dendritic cells from chronic hepatitis C virus (HCV)-infected non-responders to interferon/ribavirin therapy.
Article in Journal of clinical immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Role of circulatory microRNAs in the pathogenesis of hepatitis C virus.Virusdisease · 2017Review
- Acute Liver Damage Associated with Innate Immune Activation in a Small Nonhuman Primate Model of Hepacivirus Infection.Journal of virology · 2016Article
- Host Genetic Factors and Dendritic Cell Responses Associated with the Outcome of Interferon/Ribavirin Treatment in HIV-1/HCV Co-Infected Individuals.Journal of clinical & cellular immunology · 2014Article
- Dendritic Cells in HIV-1 and HCV Infection: Can They Help Win the Battle?Virology : research and treatment · 2013Review
- MicroRNAs, hepatitis C virus, and HCV/HIV-1 co-infection: new insights in pathogenesis and therapy.Viruses · 2012Review
- Theoretical basis of a beneficial role for vitamin D in viral hepatitis.World journal of gastroenterology · 2012Review
- Myd88-dependent toll-like receptor 7 signaling mediates protection from severe Ross River virus-induced disease in mice.Journal of virology · 2012Article
- Review
- Dendritic cells in hepatitis C infection: can they (help) win the battle?Journal of gastroenterology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimDendritic cell (DC) dysfunction has been suggested to play a role in the weak antiviral T-cell responsiveness observed during the course of chronic hepatitis C virus (HCV) infection. This study was undertaken to evaluate whether changes in DC functions might be related to a different therapeutic outcome in HCV-infected patients.
methodsPeripheral blood DCs (PBDCs) or monocyte-derived DCs (MoDCs) were obtained from chronic HCV-infected patients, sustained virologic responders (SVR) or non-responders (NR) to interferon/ribavirin therapy, and from healthy controls (HC). The frequency of BDCA-1+, BDCA-3+ or CD16+ myeloid DCs (mDCs) and BDCA-2+ plasmacytoid DCs (pDCs), as well as the expression of the costimulatory molecule CD86 in each PBDC subset, were evaluated by flow cytometry. MoDCs from single individuals were stimulated with TLR2, TLR3, TLR4, and TLR7 ligands and analyzed for CD86, CD83, CD40, CD80, and CD209 expression. Finally, mitogen-activated protein kinase (MAPK) phosphorylation of TLR7-triggered MoDCs was assessed by Western blotting.
resultsNR exhibited a reduced percentage of BDCA-1+ mDCs, as well as lower levels of CD86+ cells, in both BDCA-1+ mDCs and pDCs as compared to SVR and HC. Furthermore, MoDCs from NR displayed a defective CD86 and CD83 increase and ERK1/2 or p38-MAPK phosphorylation upon TLR7-cell triggering.
conclusionsOur data suggest that a TLR7-dependent impairment of costimulatory molecule expression caused by HCV persistence may affect DC activity in NR patients.
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What OpenQuestion holds
Registered trials
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