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Cited by 7Hepatitis B Virus StudiesLiver physiology and pathologyHepatitis C virus research

CD163 impairs HBV clearance in mice by regulating intrahepatic T cell immune response via an IL-10-dependent mechanism

Liu, Ziying, Li, Guiping, Li, Xiaoran, Wang, Yiran, Liao, Leyi, Yang, Ti, Han, Chao, Huang, Kuiyuan +4 more·2025·Antiviral Research
DOI 10.1016/j.antiviral.2025.106093
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Abstract

Background & aims Chronic hepatitis B (CHB) arises from a persistent hepatitis B virus (HBV) infection, complicating efforts for a functional cure. Kupffer cells (KCs), liver-resident macrophages, are pivotal in mediating immune tolerance to HBV. Although CD163 marks M2-polarized KCs, its precise role in HBV infection remains unclear and warrants further investigation. Methods CD163 expression in liver tissues of patients with CHB was analyzed using the Gene Expression Omnibus (GEO) database. Cd163 knockout mice were utilized to establish HBV-persistent mouse model, and CD163 deficiency effect on HBV viral markers and T cell immune responses were examined in vivo and in vitro. Results CD163 expression was elevated and correlated with ALT levels in the liver of patients with CHB. In HBV-persistent mouse model, CD163 deficiency facilitated the clearance of HBsAg, HBeAg, HBV DNA, and HBcAg. Additionally, CD163 deficiency promoted the differentiation of naïve T cells into HBV-specific effector T cells. Further, we found that CD163 deficiency reduces KCs-derived IL-10 secretion, and blocking IL-10 further strengthens the enhanced HBV-specific T cell response due to CD163 deficiency. Conclusions Our findings indicate that CD163 deficiency enhances the HBV-specific T cell response, thereby facilitating HBV clearance through reducing KCs-derived IL-10 secretion. This suggests that CD163 may serve as a potential target for the restoration of exhausted T cell function.

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  • In chronic viral hepatitis or parasitic infections, excessive anti-inflammatory polarization may impair pathogen clearance and perpetuate chronic inflammation.

    “In these settings, excessive anti-inflammatory polarization may impair pathogen clearance and perpetuate chronic inflammation, thereby reshaping macrophage function (129–135).”

    From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [130]

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Authors
Liu, Z., Li, G., Li, X., Wang, Y., Liao, L., Yang, T., Han, C., Huang, K., Chen, C., Li, X., Liu, H., & Zhang, X.
Affiliations
  • Nanfang Hospital (CN)
  • Second Affiliated Hospital of Nanchang University (CN)
Corresponding author
  • Liu, Ziying
  • Liu, Hongyan
  • Zhang, Xiaoyong
ORCID
Venue
Antiviral Research
Publisher
Elsevier BV
Published
2025-03
Volume
235
Pages
106093
ISSN
0166-3542 (ISSN-L)
DOI
10.1016/j.antiviral.2025.106093
OpenAlex
W4406714590
Cited by
7
References
45
Citations by year
2026: 5 · 2025: 2
FWCI
4.85
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Antiviral Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China
  • Special Project for Research and Development in Key Areas of Guangdong Province
Topics
  • Health Sciences › Medicine › Epidemiology › Hepatitis B Virus Studies
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Hepatology › Hepatitis C virus research
Keywords
CD163, hepatitis B virus, chronic hepatitis B, Kupffer cells, M2 macrophage polarization, IL-10, HBV-specific T cell responses, T cell exhaustion, HBV clearance, persistent HBV infection, hepatic macrophages
MeSH terms
CD163 Antigen, Animals, Disease Models, Animal, Female, Hepatitis B Surface Antigens, Hepatitis B virus, Humans, Kupffer Cells, Liver, Male, Mice, Inbred C57BL, Receptors, Cell Surface, T-Lymphocytes, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Interleukin-10, Mice, Knockout, Hepatitis B, Chronic, Mice

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