ReviewJournal of immunology research2026
Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.
Review in Journal of immunology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sustained elevation of hepatitis B surface antigen (HBsAg) facilitates the progression of chronic hepatitis B virus (HBV) pathogenesis, and initiates and sustains host immune tolerance. Immune tolerance is a major factor contributing to viral persistence and viral clearance failure. HBsAg exerts regulatory effects on innate defenses and adaptive responses, limiting the activity of dendritic cells (DCs), natural killer (NK) cells, monocytes/macrophages, T lymphocytes, and B cells. Furthermore, it fosters a tolerogenic environment via interconnected regulatory cell networks, immune checkpoint molecules, and anti-inflammatory cytokines. HBsAg can enhance the intrahepatic immune-tolerant (IT) microenvironment by downregulating costimulatory molecules and promoting the secretion of immunosuppressive cytokines by intrahepatic nonparenchymal cells. This review systematically summarizes how HBsAg interferes with immune cell function and signaling pathways to establish a tolerogenic environment. We also cover recent progress in treatments that target HBsAg-induced immune tolerance. This review establishes a solid theoretical foundation and identifies new therapeutic approaches that can break tolerance to achieve a functional cure for chronic hepatitis B (CHB).
Indexed as
Identifiers
What OpenQuestion holds
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.