ArticleJournal of microbiology (Seoul, Korea)2015
Regulation of HBV-specific CD8(+) T cell-mediated inflammation is diversified in different clinical presentations of HBV infection.
Article in Journal of microbiology (Seoul, Korea), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Pooled it
- Tumor-associated macrophages and CD8+ T cells: dual players in the pathogenesis of HBV-related HCC.Frontiers in immunology · 2024Review
- Changes in the IL-18, IL-22, and T lymphocyte subset levels in patients with hepatitis B-related liver cirrhosis and their predictive values for hepatorenal syndrome.American journal of translational research · 2023Article
- Insights into the Relationship between Pentraxin-3 and Cancer.International journal of molecular sciences · 2022Review
- Hepatitis B Flare in Hepatitis B e Antigen-Negative Patients: A Complicated Cascade of Innate and Adaptive Immune Responses.International journal of molecular sciences · 2022Review
- Soluble programmed cell death-1 predicts hepatocellular carcinoma development during nucleoside analogue treatment.Scientific reports · 2022Article
- Increase in Serum Soluble Tim-3 Level Is Related to the Progression of Diseases After Hepatitis Virus Infection.Frontiers in medicine · 2022Article
- Serum pentraxin 3 as a biomarker of hepatocellular carcinoma in chronic hepatitis B virus infection.Scientific reports · 2020Observational
- High lymphocyte‑to‑monocyte ratio is associated with low α‑fetoprotein expression in patients with hepatitis B virus‑associated hepatocellular carcinoma.Molecular medicine reports · 2020Article
- Immune Checkpoints in Viral Infections.Viruses · 2020Review
- Tim-3 expression and its role in hepatocellular carcinoma.Journal of hematology & oncology · 2018Review
- Association of viral hepatitis and bipolar disorder: a nationwide population-based study.Journal of translational medicine · 2018Article
- Highly elevated soluble Tim-3 levels correlate with increased hepatocellular carcinoma risk and poor survival of hepatocellular carcinoma patients in chronic hepatitis B virus infection.Cancer management and research · 2018Article
- Article
- Impaired Subset Progression and Polyfunctionality of T Cells in Mice Exposed to Methamphetamine during Chronic LCMV Infection.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic HBV infection is the leading cause of liver cirrhosis and hepatic cancer, but the individual responses toward HBV infection are highly variable, ranging from asymptomatic to chronic active hepatitis B inflammation. In this study, we hypothesized that the different individual responses to HBV infection was associated with differences in HBV-specific CD8(+) T cell-mediated inflammation and cytotoxicity. Blood samples were collected from subjects with asymptomatic HBV-infection, subjects undergoing active chronic HBV flares (active CHB), and subjects with HBV-infected hepatocellular carcinoma (HBV-HCC). By tetramer staining, we found that all three groups had similar frequencies of HBVspecific CD8(+) T cells. However, after HBV peptide stimulation, the HBV-specific CD8(+) T cells in asymptomatic subjects had significantly stronger interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), and CD107a expression than those in active CHB and HBV-HCC patients. Examination of surface marker expression revealed that the PD-1(-)Tim-3(-) double-negative cell population was the main contributor to HBV-specific inflammation. In active CHB patients and HBV-HCC patients, however, the frequencies of activated PD-1(-)Tim-3(-) cells were significantly reduced. Moreover, the serum HBV DNA titer was not correlated with the frequencies of HBV-specific CD8(+) T cells but was inversely correlated with the frequencies of IFN-g-expressing and CD107a-express cells in response to HBV stimulation. Together, our data demonstrated that the status of HBVspecific CD8(+) T cell exhaustion was associated with different clinical outcomes of chronic HBV infection.
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Registered trials
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