ArticleScientific reports2024
The hijacking of HBV by small extracellular vesicles inhibits M1 macrophages to facilitate immune evasion.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Macrophages in oncoviral infections: from immune regulators to therapeutic targets.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Extracellular Vesicles in Liver Disease: Redefining Diagnostic and Therapeutic Strategies.International journal of stem cells · 2026Review
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- Review
- Intercellular highways of viral spread: tunneling nanotubes and extracellular vesicles at the maternal-fetal interface.Current opinion in virology · 2025Review
- A Primer on Proteomic Characterization of Intercellular Communication in a Virus Microenvironment.Molecular & cellular proteomics : MCP · 2025Review
- Ethanol Disrupts the Protective Crosstalk Between Macrophages and HBV-Infected Hepatocytes.Biomolecules · 2025Article
- Protein swarm-based cause-effect analysis: effects of microRNAs on cooperation networks linking COVID-19 infections, atherosclerosis, and Alzheimer's disease.Frontiers in cardiovascular medicine · 2025Article
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small extracellular vesicles (sEVs) have the ability to transfer genetic material between cells, but their role in mediating HBV infection and regulating M1 macrophages to promote immune evasion remains unclear. In this study, we utilized PMA + LPS + IFN-γ to induce THP-1 into M1 macrophages. We then extracted sEVs from HepG2.2.15 cell and treated the M1 macrophages with these sEVs. QPCR detection revealed the presence of HBV-DNA in the M1 macrophages. Additionally, RT-qPCR and WB analysis demonstrated a significantly decreased in the expression of TLR4, NLRP3, pro-caspase-1, caspase-1p20, IL-1β and IL-18 in the M1 macrophages (P < 0.05). Furthermore, RT-qPCR results displayed high expression levels of that miR-146a and FEN-1 in the sEVs derived from HepG2.2.15 cells (P < 0.01). RT -qPCR and WB analysis showed that these sEVs enhanced the expression of FEN-1 or miR-146a in the M1 macrophages through miR-146a or FEN-1 (P < 0.05), while simultaneously reducing the expression of TLR4, NLRP3, caspase-1p20, IL-1β and IL-18 in the M1 macrophages (P < 0.05). In summary, our findings indicate that sEVs loaded with HBV inhibit the inflammatory function of M1 macrophages and promote immune escape. Additionally, miR-146a and FEN-1 present in the sEVs play a crucial role in this process.
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