Nucleos(t)ide analogues potentially activate T lymphocytes through inducing interferon expression in hepatic cells and patients with chronic hepatitis B.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
25 Oct 2024
Historique:
received: 06 05 2024
accepted: 11 10 2024
medline: 26 10 2024
pubmed: 26 10 2024
entrez: 25 10 2024
Statut: epublish

Résumé

Chronic hepatitis B (CHB) leads to liver inflammation and dysfunction, resulting in liver fibrosis and cancer. Nucleos(t)ide analogues (NAs), inhibitors of hepatitis B virus (HBV), specifically suppress HBV replication. We proposed that immune modulation benefits seroconversion by HBsAg loss. However, activation of T lymphocytes also deteriorates hepatic inflammation. Therefore, we intended to investigate the T cell status and its relationship with hepatic functions in CHB patients treated with NAs. Serum markers, including liver function markers AST, ALT, and HBV-infected markers HBV DNA, HBsAg, HBeAg, and HBsAb were measured in the clinical routine. The T cell levels and markers, including CD69, CD107a, CXCR3, and PD-1 were investigated using flow cytometry. Meanwhile, IFNγ, IL-2, and CXCL10 as immune activation markers in the PBMCs were investigated using qPCR. To validate the effects of NAs on T cell status, qPCR and flow cytometry were used to investigate the gene expression in the HepG2 and PLC5 cells treated with NAs, and in the healthy PBMCs treated with the cell-cultured supernatant. We found that NAs significantly suppressed HBV DNA and reduced AST and ALT levels in the CHB patients. Meanwhile, AST and ALT were both positively correlated with activation marker CD107a in CD8

Identifiants

pubmed: 39455685
doi: 10.1038/s41598-024-76270-8
pii: 10.1038/s41598-024-76270-8
doi:

Substances chimiques

Antiviral Agents 0
Interferons 9008-11-1
Nucleosides 0
DNA, Viral 0
Alanine Transaminase EC 2.6.1.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

25286

Subventions

Organisme : Cheng Hsin General Hospital, Taiwan
ID : CHGH113-112-N03
Organisme : National Science and Technology Council
ID : NSTC 112-2314-B-182-048
Organisme : Chang Gung University, Taiwan
ID : UMRPD1N0091

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Ai-Sheng Ho (AS)

Division of Gastroenterology, Cheng Hsin General Hospital, Taipei, 112, Taiwan.

Jungshan Chang (J)

Graduate Institute of Medical Sciences, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan. js.chang@tmu.edu.tw.

Shou-Dong Lee (SD)

Division of Gastroenterology, Cheng Hsin General Hospital, Taipei, 112, Taiwan.

Zong-Lin Sie (ZL)

Research Center of Radiation Medicine, Chang Gung University, Taoyuan, 333, Taiwan.

Hui-Fen Shih (HF)

Division of Gastroenterology, Cheng Hsin General Hospital, Taipei, 112, Taiwan.

Chun Yeh (C)

Division of Gastroenterology, Cheng Hsin General Hospital, Taipei, 112, Taiwan.

Cheng-Liang Peng (CL)

Department of Isotope Application Research, National Atomic Research Institute, Taoyuan, 325, Taiwan.

Kapil Dev (K)

Research Center of Radiation Medicine, Chang Gung University, Taoyuan, 333, Taiwan.

Chun-Chia Cheng (CC)

Research Center of Radiation Medicine, Chang Gung University, Taoyuan, 333, Taiwan. cccheng.biocompare@gmail.com.
Division of Pulmonary Oncology and Interventional Bronchoscopy, Department of Thoracic Medicine, Chang Gung Memorial Hospital, Linkou, Taoyuan, 333, Taiwan. cccheng.biocompare@gmail.com.

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