ArticleNature medicine2015
Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 1 of them a synthesis that pooled it.
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
152 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.
- Hepatitis B infection and intrahepatic cholestasis of pregnancy: A systematic review and meta-analysis.Medicine · 2020Pooled it
- Therapeutic Potential of TLR8 Agonist GS-9688 (Selgantolimod) in Chronic Hepatitis B: Remodeling of Antiviral and Regulatory Mediators.Hepatology (Baltimore, Md.) · 2021Trial
- Memory Regulatory T cells Increase Only In Inflammatory Phase of Chronic Hepatitis B Infection and Related to Galectin-9/Tim-3 interaction.Scientific reports · 2017Trial
- Review
- TUFT1 stabilizes TGF-β receptor II protein and facilitates activation of hepatic stellate cells into metastasis-promoting myofibroblasts.Cell death and differentiation · 2026Article
- The competition of amino acid among tumors, tumor-associated macrophages and T cells based on metabolic reprogramming.iScience · 2026Review
- T cell adaptation in chronic infections and tumors.Cellular & molecular immunology · 2026Review
- Targeting the innate immune system in treating hepatitis B: prospects for functional cure.Clinical and molecular hepatology · 2026Review
- From exhaustion to functional cure: frontiers in reversing HBV-specific T-cell immunity.Frontiers in immunology · 2026Review
- Fine needle aspirates characterise the hepatocellular carcinoma immune niche to predict immune checkpoint inhibitor outcomes.JHEP reports : innovation in hepatology · 2026Article
- The immunoecology of occult hepatitis B virus infection: genetic remodeling and the immune-mediated microcosm.Frontiers in immunology · 2026Review
- PD-L1Frontiers in immunology · 2026Article
- IL-21 attenuates liver inflammation by enhancing myeloid-derived suppressor cells immunosuppressive function in chronic HBV infection.Journal of translational medicine · 2025Article
- The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Tissue-resident memory CD8Nature reviews. Gastroenterology & hepatology · 2025Review
- Scientific and medical evidence informing expansion of hepatitis B treatment guidelines.The lancet. Gastroenterology & hepatology · 2025Review
- Immunological Landscape and Molecular Therapeutic Targets of the Tumor Microenvironment in Hepatocellular Carcinoma.International journal of molecular sciences · 2025Review
- Interaction of low-density neutrophils with other immune cells in the mechanism of inflammation.Molecular medicine (Cambridge, Mass.) · 2025Review
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
- Harnessing nanoparticles for reshaping tumor immune microenvironment of hepatocellular carcinoma.Discover oncology · 2025Review
92 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
Abstract
Infection with hepatitis B virus (HBV) results in disparate degrees of tissue injury: the virus can either replicate without pathological consequences or trigger immune-mediated necroinflammatory liver damage. We investigated the potential for myeloid-derived suppressor cells (MDSCs) to suppress T cell-mediated immunopathology in this setting. Granulocytic MDSCs (gMDSCs) expanded transiently in acute resolving HBV, decreasing in frequency prior to peak hepatic injury. In persistent infection, arginase-expressing gMDSCs (and circulating arginase) increased most in disease phases characterized by HBV replication without immunopathology, whilst L-arginine decreased. gMDSCs expressed liver-homing chemokine receptors and accumulated in the liver, their expansion supported by hepatic stellate cells. We provide in vitro and ex vivo evidence that gMDSCs potently inhibited T cells in a partially arginase-dependent manner. L-arginine-deprived T cells upregulated system L amino acid transporters to increase uptake of essential nutrients and attempt metabolic reprogramming. These data demonstrate the capacity of expanded arginase-expressing gMDSCs to regulate liver immunopathology in HBV infection.
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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.