ArticleHepatology international2024
HBeAg induces neutrophils activation impairing NK cells function in patients with chronic hepatitis B.
Article in Hepatology international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- The crucial role of RIG-I in upregulating neutrophil CXCR2 expression through the MAPK signaling pathway in viral pneumonia.Respiratory research · 2026Article
- The clinical significance and optimization strategies of HBeAg seroclearance in chronic hepatitis B treatment.Frontiers in cellular and infection microbiology · 2026Review
- Innate immune recognition in hepatitis B virus infection.Virulence · 2025Review
- Hepatitis B Virus e Antigen in Mother-to-Child Transmission and Clinical Management of Hepatitis B.Viruses · 2025Review
- IL-1b-Bearing NETs: Bridging Inflammation to Early Cirrhosis in Hepatitis B.International journal of molecular sciences · 2025Article
- [Current status of research on the impairment of natural killer cell function caused by hepatitis B virus infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe role of neutrophils in hepatitis B virus (HBV) infection has been a subject of debate due to their involvement in antiviral responses and immune regulation. This study aimed to elucidate the neutrophil characteristics in patients with chronic hepatitis B (CHB).
methodsThrough flow cytometry and ribonucleic acid-sequencing analysis, the phenotypes and counts of neutrophils were analyzed in patients with CHB. Moreover, the effects of HBeAg on neutrophils and the corresponding pattern recognition receptors were identified. Simultaneously, the cross-talk between neutrophils and natural killer (NK) cells was investigated.
resultsNeutrophils were activated in patients with CHB, characterized by higher expression levels of programmed death-ligand 1 (PD-L1), cluster of differentiation 86, and interleukin-8, and lower levels of CXC motif chemokine receptor (CXCR) 1 and CXCR2. Hepatitis B e antigen (HBeAg) partially induces neutrophil activation through the Toll-like receptor 2 (TLR2). A consistent upregulation of the TLR2 and HBeAg expression was observed in patients with CHB. Notably, the genes encoding molecules pivotal for NK-cell function upon NK receptor engagement enriched in neutrophils after HBeAg activation. The HBeAg-activated neutrophils demonstrated the ability to decrease the production of interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) in NK cells, while the PD-1 and PD-L1 pathways partially mediated the immunosuppression.
conclusionsThe immunosuppression of neutrophils induced by HBeAg suggests a novel pathogenic mechanism contributing to immune tolerance in patients with CHB.
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