ArticleHepatology (Baltimore, Md.)2015
Hepatitis C virus-induced reduction in miR-181a impairs CD4(+) T-cell responses through overexpression of DUSP6.
Article in Hepatology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- MicroRNA Control of Hepatocyte-Stromal Crosstalk in the Early Premalignant Microenvironment of HBV-Associated HCC.International journal of molecular sciences · 2026Review
- DUSP6 ablation restores CAR T-cell fitness impaired by tumor CD58 loss through invigoration of AP-1 signaling.Signal transduction and targeted therapy · 2026Article
- ATM in immunobiology: From lymphocyte development to cancer immunotherapy.Translational oncology · 2025Review
- Review
- MicroRNAs in infectious diseases: potential diagnostic biomarkers and therapeutic targets.Clinical microbiology reviews · 2023Review
- A DUSP6 inhibitor suppresses inflammatory cardiac remodeling and improves heart function after myocardial infarction.Disease models & mechanisms · 2023Article
- Article
- Micro-Players of Great Significance-Host microRNA Signature in Viral Infections in Humans and Animals.International journal of molecular sciences · 2022Review
- Article
- Mitochondrial topoisomerase 1 inhibition induces topological DNA damage and T cell dysfunction in patients with chronic viral infection.Frontiers in cellular and infection microbiology · 2022Article
- Bone Mesenchymal Stem Cell-Derived Exosome-Enclosed miR-181a Induces CD4Journal of oncology · 2022Article
- miR-181a-regulated pathways in T-cell differentiation and aging.Immunity & ageing : I & A · 2021Review
- BCI Suppresses RANKL-Mediated Osteoclastogenesis and Alleviates Ovariectomy-Induced Bone Loss.Frontiers in pharmacology · 2021Article
- LncRNA HOTAIRM1 promotes MDSC expansion and suppressive functions through the HOXA1-miR124 axis during HCV infection.Scientific reports · 2020Article
- miR-27b-mediated suppression of aquaporin-11 expression in hepatocytes reduces HCV genomic RNA levels but not viral titers.Virology journal · 2019Article
- Article
- Disruption of Telomere Integrity and DNA Repair Machineries by KML001 Induces T Cell Senescence, Apoptosis, and Cellular Dysfunctions.Frontiers in immunology · 2019Article
- Topological DNA damage, telomere attrition and T cell senescence during chronic viral infections.Immunity & ageing : I & A · 2019Article
- Inhibition of TRF2 accelerates telomere attrition and DNA damage in naïve CD4 T cells during HCV infection.Cell death & disease · 2018Article
- DUSP6 mediates T cell receptor-engaged glycolysis and restrains TProceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
unlabelledT cells play a crucial role in viral clearance or persistence; however, the precise mechanisms that control their responses during viral infection remain incompletely understood. MicroRNA (miR) has been implicated as a key regulator controlling diverse biological processes through posttranscriptional repression. Here, we demonstrate that hepatitis C virus (HCV)-mediated decline of miR-181a expression impairs CD4(+) T-cell responses through overexpression of dual specific phosphatase 6 (DUSP6). Specifically, a significant decline of miR-181a expression along with overexpression of DUSP6 was observed in CD4(+) T cells from chronically HCV-infected individuals compared to healthy subjects, and the levels of miR-181a loss were found to be negatively associated with the levels of DUSP6 overexpression in these cells. Importantly, reconstitution of miR-181a or blockade of DUSP6 expression in CD4(+) T cells led to improved T-cell responses including enhanced CD25 and CD69 expression, increased interleukin-2 expression, and improved proliferation of CD4(+) T cells derived from chronically HCV-infected individuals.
conclusionSince a decline of miR-181a concomitant with DUSP6 overexpression is the signature marker for age-associated T-cell senescence, these findings provide novel mechanistic insights into HCV-mediated premature T-cell aging through miR-181a-regulated DUSP6 signaling and reveal new targets for therapeutic rejuvenation of impaired T-cell responses during chronic viral infection.
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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.