ArticleFrontiers in immunology2025
PD-L1 in plasmacytoid dendritic cells promote HBV persistence through disrupting humoral immune response.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.Journal of immunology research · 2026Review
- Highly Alkaline-ResistantMicroorganisms · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To investigate the efficacy of PD-L1 blockade in restoring humoral immune response against HBV. Methods: HBV-persistent C57BL/6J mice were established through hydrodynamic tail vein injection of 10 µg pAAV-HBV1.2 plasmid. Subsequently, mice treated i.p. with anti-PD-L1 and/or anti-CTLA-4 at specified time points, with dosages of 500 µg, 250 µg, and 250 µg, respectively. Additionally, 5 × 10 Results: PD-L1 blockade markedly enhanced the differentiation of Tfh cells and GC B cells in HBV-persistent C57BL/6J mice, thereby promoting HBV clearance. Additionally, pDCs exhibited an increased capacity to induce immune tolerance, with pDCs isolated from HBV carriers inducing viral persistence. This persistence was effectively counteracted by treatment with anti-PD-L1. Conclusion: pDCs mediate the dysregulation of the humoral immune response to HBV through PD-L1 in chronic hepatitis B infection, highlighting a promising target for the management of chronic HBV.
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Registered trials
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