ArticleHepatology international2022
Reduction of natural killer cells is associated with poor outcomes in patients with hepatitis B virus-related acute-on-chronic liver failure.
Article in Hepatology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Uncovering immune dysfunction in ACLF: Cellular mechanisms, molecular pathways, and therapeutic frontiers.Journal of hepatology · 2026Review
- [Analyzing research advances in single-cell sequencing technology for immunopathological mechanisms in acute-on-chronic liver failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Expression of CD38Scientific reports · 2026Article
- The Dual Role of IP-10/CXCL10 in Liver Injury: From Pathogenic Mediator to Clinical Biomarker and Therapeutic Target.Drug design, development and therapy · 2026Review
- Mesenchymal Stem Cells Ameliorate Acute-on-Chronic Liver Failure Associated With Expansion of Immunoregulatory Hepatic NKp46Journal of immunology research · 2026Article
- The Predictive Role of the Systemic Inflammation Response Index in the Prognosis of Hepatitis B Virus-Related Acute-on-Chronic Liver Failure: A Multicenter Study.Healthcare (Basel, Switzerland) · 2025Article
- Potential Biomarkers and Therapeutic Targets in Hepatitis B Virus-related Acute Liver Failure: Interplay of the Ferroptosis, Autophagy and Immune Responses.International journal of medical sciences · 2025Article
- The Impact of Liver Failure on the Immune System.International journal of molecular sciences · 2024Review
- Characteristics of circulating immune cells in HBV-related acute-on-chronic liver failure following artificial liver treatment.BMC immunology · 2023Article
- The Important Roles of Natural Killer Cells in Liver Fibrosis.Biomedicines · 2023Review
- Comparative analysis of monocyte-derived dendritic cell phenotype and T cell stimulatory function in patients with acute-on-chronic liver failure with different clinical parameters.Frontiers in immunology · 2023Article
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Authors and funding
24 authors at 4 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsNatural killer (NK) cells are critical innate effectors that respond to viral infections and contribute to immunopathology. Here, we aimed to investigate the role of NK cells in hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) and elucidate the underlying mechanism by examining their phenotypic and functional profiles.
methodsWe included patients with HBV-ACLF (n = 37) and chronic hepatitis B (n = 19), and healthy controls (n = 13) in our study. We examined the phenotype and function of different subsets of peripheral NK cells using flow cytometry and RNA-sequencing analysis, and screened liver NK cells using immunohistochemistry. We detected inflammatory cytokines using a Luminex assay. In addition, we analyzed the relationships between these parameters and disease severity.
resultsPeripheral NK cells were decreased and characterized by high expression of caspase-3, Ki67, CXCR3, NKG2D, NKp46, CD107a, and GM-CSF, and typified by higher cell migration and immune response by RNA-sequencing analysis in patients with HBV-ACLF than in those with chronic hepatitis B. Accumulations of CXCL-10 and NK cells were found in the liver, and excessive production of CXCL-10 in the peripheral blood contributed to the apoptosis of NK cells in vitro. The decrease in NK cells was associated with the level of HBV DNA and disease severity and had good prognostic performance in predicting the outcome of patients with HBV-ACLF through AUROC analysis.
conclusionNK cells were significantly decreased and showed dysfunction of phenotypic and functional profiles across distinct subsets in the peripheral blood of patients with ACLF. Crosstalk between CXCL-10 and NK cells may mediate the unbalanced distribution of NK cells. Understanding the dysfunction and decrease in NK cells may provide new insights into ACLF pathogenesis.
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