ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Viral-Directed Augmentation of Kupffer Cell Cross-Presentation Provokes Antitumor Immunity Against Liver Metastasis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
- Colorectal cancer liver metastases: mechanism and therapy.Frontiers in immunology · 2026Review
- Transcriptomic profiling of Kupffer cells exposed toFood and waterborne parasitology · 2025Article
- Viral-Directed Augmentation of Kupffer Cell Cross-Presentation Provokes Antitumor Immunity Against Liver Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
9 authors.
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Abstract
Liver metastasis is associated with poor prognosis and resistance to immune checkpoint inhibitors. Functional modulation of Kupffer cells (KCs) holds promise as an alternative immunotherapeutic approach. Leveraging their capacity to capture circulating virions, an oncolytic virus-based KC-targeting strategy is developed that demonstrated efficacy and safety in treating multifocal liver metastasis. A single intravenous infusion of the M51R mutant vesicular stomatitis virus (VSV-M51R), but not wild-type (WT) VSV, induced significant tumor regression in mouse models of forced liver metastasis, independent of direct oncolysis. The ineffectiveness of VSV-WT is attributed to its induction of massive KC apoptosis, whereas VSV-M51R replicated transiently within KCs without compromising viability. Instead, VSV-M51R promoted KC proliferation in tumor-adjacent areas, enhancing their access to tumor foci and cross-presentation of tumor antigens. This led to robust activation of hepatic anti-tumor CD8
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