ArticleJournal for immunotherapy of cancer2024
Therapeutic inhibition of monocyte recruitment prevents checkpoint inhibitor-induced hepatitis.
Article in Journal for immunotherapy of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Heterogeneity of macrophages in PD-1/PD-L1 inhibitor therapy: a single-cell perspective.Cellular & molecular biology letters · 2026Review
- Single-cell transcriptomics unveils the immunologic landscape of anti-PD-1-associated indirect drug-induced liver injury.Journal of gastroenterology · 2026Article
- Circulating exhausted CD8+ effector memory cells differentiate immune checkpoint inhibitor-induced liver injury from other acute immune-mediated liver injuries.Journal for immunotherapy of cancer · 2026Article
- Role of innate immunity in the development of cancer immunotherapy immune-mediated adverse events.Frontiers in immunology · 2026Review
- The role of metabolites in the causal effect of immune cell phenotypes on immunotherapy toxicity risk.Discover oncology · 2025Article
- Immune-mediated liver injury from checkpoint inhibitors: mechanisms, clinical characteristics and management.Nature reviews. Gastroenterology & hepatology · 2025Review
- Targeting molecular pathways to control immune checkpoint inhibitor toxicities.Trends in immunology · 2025Review
- The broad spectrum of cancer and immunotherapy: achievements and limitations.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCheckpoint inhibitor-induced hepatitis (CPI-hepatitis) is an emerging problem with the widening use of CPIs in cancer immunotherapy. Here, we developed a mouse model to characterize the mechanism of CPI-hepatitis and to therapeutically target key pathways driving this pathology.
methodsC57BL/6 wild-type (WT) mice were dosed with toll-like receptor (TLR)9 agonist (TLR9-L) for hepatic priming combined with anti-cytotoxic T lymphocyte antigen-4 (CTLA-4) plus anti-programmed cell death 1 (PD-1) ("CPI") or phosphate buffered saline (PBS) control for up to 7 days. Flow cytometry, histology/immunofluorescence and messenger RNA sequencing were used to characterize liver myeloid/lymphoid subsets and inflammation. Hepatocyte damage was assessed by plasma alanine transaminase (ALT) and cytokeratin-18 (CK-18) measurements
resultsCo-administration of combination CPIs with TLR9-L induced liver pathology closely resembling human disease, with increased infiltration and clustering of granzyme B
conclusionThis newly established mouse model provides a platform for
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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 Socratic graph.