Trial reportPLoS pathogens2013
Hepatitis B virus induces IL-23 production in antigen presenting cells and causes liver damage via the IL-23/IL-17 axis.
Trial report in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Association of IL-23R Polymorphisms (rs6682925, rs10889677, rs1884444) With Cancer Risk: A PRISMA-Compliant Meta-Analysis.Medicine · 2015Pooled it
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Interleukin-17A signaling promotes CD8+ T cell cytotoxicity against West Nile virus infection through enhancing PI3K-mTOR-mediated metabolism.PLoS pathogens · 2025Article
- Infection Risk and Vaccination in the Management of Psoriasis: Considerations for Biologic Therapy.Psoriasis (Auckland, N.Z.) · 2025Review
- Role of the type 3 cytokines IL-17 and IL-22 in modulating metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Review
- The Role of Interleukins in HBV Infection: A Narrative Review.Journal of personalized medicine · 2023Review
- Insights into the impact of hepatitis B virus on hepatic stellate cell activation.Cell communication and signaling : CCS · 2023Review
- ILC3s restrict the dissemination of intestinal bacteria to safeguard liver regeneration after surgery.Cell reports · 2023Article
- Microbial Components and Effector Molecules in T Helper Cell Differentiation and Function.Immune network · 2023Review
- The Double Game Played by Th17 Cells in Infection: Host Defense and Immunopathology.Pathogens (Basel, Switzerland) · 2022Review
- Perivascular Mesenchymal Stem/Stromal Cells, an Immune Privileged Niche for Viruses?International journal of molecular sciences · 2022Review
- Monocytic MDSCs homing to thymus contribute to age-related CD8+ T cell tolerance of HBV.The Journal of experimental medicine · 2022Article
- Review
- Association Between Serum IL-6, IL-10, IL-12, and IL-23 Levels and Severity of Liver Cirrhosis.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2021Observational
- IL-17 in the Pathogenesis of Disease: Good Intentions Gone Awry.Annual review of immunology · 2021Review
- IFN-γ facilitates liver fibrogenesis by CD161Clinical & translational immunology · 2021Article
- Cytokines and Chemokines in HBV Infection.Frontiers in molecular biosciences · 2021Review
- In vivo and in vitro Evaluation of Cytokine Expression Profiles During Middle East Respiratory Syndrome Coronavirus (MERS-CoV) Infection.Journal of inflammation research · 2021Article
- Transcriptome Classification Reveals Molecular Subgroups in Patients with Hepatitis B Virus.Computational and mathematical methods in medicine · 2021Article
- Macrophage Phenotypes and Hepatitis B Virus Infection.Journal of clinical and translational hepatology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-23 regulates myriad processes in the innate and adaptive immune systems, and is a critical mediator of the proinflammatory effects exerted by Th17 cells in many diseases. In this study, we investigated whether and how hepatitis B virus (HBV) causes liver damage directly through the IL-23 signaling pathway. In biopsied liver tissues from HBV-infected patients, expression of both IL-23 and IL-23R was remarkably elevated. In vivo observations also indicated that the main sources of IL-23 were myeloid dendritic cells (mDCs) and macrophages. Analysis of in vitro differentiated immature DCs and macrophages isolated from healthy donors revealed that the HBV surface antigen (HBsAg) efficiently induces IL-23 secretion in a mannose receptor (MR)-dependent manner. Culture with an endosomal acidification inhibitor and the dynamin inhibitor showed that, upon binding to the MR, the HBsAg is taken up by mDCs and macrophages through an endocytosis mechanism. In contrast, although the HBV core antigen (HBcAg) can also stimulate IL-23 secretion from mDCs, the process was MR- and endocytosis-independent. In addition, IL-23 was shown to be indispensible for HBsAg-stimulated differentiation of naïve CD4(+) T cells into Th17 cells, which were determined to be the primary source of IL-17 in HBV-infected livers. The cognate receptor, IL-17R, was found to exist on the hepatic stellate cells and mDCs, both of which might represent the potential target cells of IL-17 in hepatitis B disease. These data provide novel insights into a yet unrecognized mechanism of HBV-induced hepatitis, by which increases in IL-23 expression, through an MR/endocytosis-dependent or -independent manner, produce liver damage through the IL-23/IL-17 axis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.