ArticleMolecular therapy. Oncology2025
Engineered oncolytic virus OH2-FLT3L enhances antitumor immunity via dendritic cell activation.
Article in Molecular therapy. Oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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
2 citing papers in PubMed.
- Intratumoral delivery of FLT3L with CXCR3/CCR5 ligands promotes XCR1Nature communications · 2025Article
- Oncolytic virus and immunogenic cell death in cancer therapy.Tumour virus research · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The combination of oncolytic viruses (OVs) with other immunotherapies, such as immunostimulatory therapies, is a current research hotspot; however, optimizing their therapeutic potential remains to be fully explored. Here, we designed a novel oncolytic herpes simplex virus 2 expressing Fms-like tyrosine kinase 3 ligand (OH2-FLT3L), which induces an antitumor cytotoxic T cell immune response by activating dendritic cells (DCs). We found that OH2-FLT3L specifically infects tumor cells, induces immunogenic cell death (ICD), and releases a large number of tumor-specific antigens, which bound to danger signals and facilitated antigenic cross-presentation by DCs, significantly enhancing T cell activation and function. Experimental results showed that OH2-FLT3L significantly increased the proportion of activated DCs, enhanced the antitumor immune response, and effectively converted "cold" tumors into "hot" tumors. In addition, when combined with anti-PD-1 antibody, OH2-FLT3L further enhanced therapeutic efficacy. In conclusion, OH2-FLT3L, as a novel oncolytic virus, demonstrates the potential to enhance antitumor immune responses through DC activation.
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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.