ReviewJournal of clinical and translational research2017
Immune mechanisms of idiosyncratic drug-induced liver injury.
Review in Journal of clinical and translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- The gut-liver axis in drug-induced liver injury (DILI): Interplay between gut microbiota, intestinal barrier, and immune system.Acta pharmaceutica Sinica. B · 2026Review
- Insights into the Biochemical and Immune Mechanisms in Drug-Induced Liver Injury Pathogenesis.Chemical research in toxicology · 2026Review
- RUCAM-ascertained immunology and autoimmunity specifics of six idiosyncratic drug-induced liver injury types with refined classification: their individual complex molecular interplay.Frontiers in immunology · 2026Review
- Trained immunity as a systemic bridge: the liver-gut-immune-oral axis in the comorbidity of chronic liver disease and periodontitis.Frontiers in immunology · 2026Review
- Corticosteroid-responsive portal lymphadenopathy mimicking malignant progression induced by furmonertinib in EGFR-mutated NSCLC: a case report.Frontiers in pharmacology · 2026Article
- The deglycosylated metabolite of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D- glucoside contributes to immune-mediated hepatotoxicity induced by Polygonum multiflorum.Archives of toxicology · 2025Article
- Autologous Organoid-T Cell Co-Culture Platform for Modeling of Immune-Mediated Drug-Induced Liver Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Voriconazole-induced liver injury: incidence patterns and risk factors in a retrospective cohort.Antimicrobial agents and chemotherapy · 2025Article
- Drug-Induced Liver Injury-Pharmacological Spectrum Among Children.International journal of molecular sciences · 2025Review
- Navigating Drug-Induced Lung Disease (DILD): A Comprehensive Review on Management and Prevention Strategies.Cureus · 2024Review
- Acute onset nitrofurantoin-induced autoimmune hepatitis after urinary tract infection treatment.Clinical case reports · 2024Article
- Roles of Cofactors in Drug-Induced Liver Injury: Drug Metabolism and Beyond.Drug metabolism and disposition: the biological fate of chemicals · 2022Review
- Article
- Regulation of the immune tolerance system determines the susceptibility to HLA-mediated abacavir-induced skin toxicity.Communications biology · 2021Article
- Biomarkers of drug-induced liver injury: a mechanistic perspective through acetaminophen hepatotoxicity.Expert review of gastroenterology & hepatology · 2021Review
- Oxidative Stress in Drug-Induced Liver Injury (DILI): From Mechanisms to Biomarkers for Use in Clinical Practice.Antioxidants (Basel, Switzerland) · 2021Review
- The hepatotoxicity of Polygonum multiflorum: The emerging role of the immune-mediated liver injury.Acta pharmacologica Sinica · 2021Review
- Recent Advances in Models of Immune-Mediated Drug-Induced Liver Injury.Frontiers in toxicology · 2021Review
- What have we learned from animal models of idiosyncratic, drug-induced liver injury?Expert opinion on drug metabolism & toxicology · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiosyncratic drug reactions (IDRs) continue to be an important issue. Specifically, idiosyncratic drug-induced liver injury (IDILI) is the most likely IDR to lead to drug withdrawal, and it accounts for a significant portion of all cases of acute liver failure. In addition, IDRs are unpredictable and their mechanisms are not well understood. There is increasing clinical evidence that most IDILI is immune mediated. Several immune mediated mechanistic hypotheses exist such as the hapten and danger hypothesis; however, they do not completely explain the idiosyncratic nature of these reactions. Extensive mechanistic studies are needed to better understand these reactions; however, it is impossible to do controlled experiments in humans, and previous animal models did not properly model IDILI. If IDILI is immune mediated and the major factor preventing liver injury in patients is immune tolerance, then a plausible method to develop an animal model of IDILI would be to impair immune tolerance. This hypothesis has shown promise in developing valid animal models of IDILI as demonstrated by a halothane induced liver injury mouse model developed by depleting myeloid derived suppressor cells (MDSCs), as well as an amodiaquine-, isoniazid-and nevirapine-induced liver injury mouse model developed by impairing immune tolerance by blocking PD-1 and CTLA-4, two immune checkpoint inhibitors. Further characterization and validation of these models is required; however, it is likely that they will make it possible to perform mechanistic studies that have been impossible in the past.
Indexed as
Identifiers
30873473PMC6410666W2591690158What 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.