ArticleMolecular cancer therapeutics2025
Blocking Feedback Immunosuppression of Antigen Presentation in Brain Tumor During Oncolytic Virotherapy with oHSV-mshPKR.
Article in Molecular cancer therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- BTK inhibition enhances immunovirotherapy in glioblastoma via tertiary lymphoid structure modulation.bioRxiv : the preprint server for biology · 2026Article
- The integrated stress response in cancer: mechanisms of tumor adaptation and therapeutic targeting.Biochemical Society transactions · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
Glioblastoma (GBM) is the most frequent malignant brain tumor. We recently discovered that oncolytic herpes simplex virus engineered to disable tumor-intrinsic protein kinase R (PKR) signaling (oHSV-shPKR) could increase oHSV oncolysis and antitumor immune response. However, in this study, we show that disabling tumor-intrinsic PKR signaling can also induce the activation of the indoleamine 2,3-dioxygenase (IDO) signaling pathway. Both GBM tumor progression and oHSV intratumoral therapy increased infiltration of IDO+CD11c+ dendritic cells (DC) into the tumor. The coculture of oHSV-infected human GBM neurospheres with monocyte-derived DCs (MoDC) dramatically increased IDO signaling activation in MoDCs through type-I IFN signaling. Addition of IDO inhibitor (indoximod) in the coculture significantly increased MoDC activation and reduced the consumption of tryptophan. Combining indoximod and oHSV significantly inhibited tumor growth and induced antigen-specific CD8+ T-cell activation. These results suggest that inhibition of the IDO pathway could significantly block feedback immunosuppression during oncolytic virotherapy of GBM.
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Registered trials
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