ArticleJournal of extracellular vesicles2026
Oncolytic Virus-Engineered Extracellular Vesicles Rewire Glioblastoma Immunity.
Article in Journal of extracellular vesicles, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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19 authors.
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Abstract
Immunotherapy with oncolytic Herpes simplex virus type 1 (oHSV-1) shows promise for glioblastoma; however, clinical benefit remains uncommon due to tumour- and host-mediated immunosuppression, which limits immune targeting of residual glioblastoma stem-like cells (GSCs). To address this barrier, extracellular vesicles (EVs) harvested from oHSV-1-infected GSCs (EVOV) were evaluated for their immunomodulatory capacity by priming peripheral blood mononuclear cells (PBMCs) ex vivo and in vivo. In GSC-PBMC organoids analysed by single-cell RNA sequencing, IFN-response and antigen-presentation programs were induced in both immune and tumour compartments, despite the GSC state. EVOV organoid transcriptome associated with patient tumour antigen-processing programs linked to improved clinical outcome, and EVOV immunopeptidomics identified candidate biomarker peptides that were also detected in patient immunopeptidomes from the clinical-trial cohort. In PBMC-engrafted NOD scid gamma mice bearing intracranial GSC xenografts, EVOV delivery increased circulating interferon (IFN) levels and enhanced systemic activation of T-cell subsets, while spatial transcriptomics revealed recruitment of peripheral immune cells to the tumour, accompanied by reprogramming of GSC states. Blocking vesicle-associated major histocompatibility complex I (MHC-I) attenuated EVOV-driven PBMC cytotoxicity against GSCs, supporting an MHC-I peptide-dependent mechanism of immune priming and a vaccine- or adjuvant-like, non-infectious, vesicle-based immunotherapeutic strategy.
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