ArticleJournal for immunotherapy of cancer2025
Oncolytic virus-induced IL-1β
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Targeting phase separation: a new strategy to disrupt the stromal-immune axis in colorectal cancer.Cell communication and signaling : CCS · 2026Review
- RBX1Cancers · 2026Article
- Innate immunity-stroma crosstalk in pancreatic cancer: overcoming spatial and metabolic barriers to immunotherapy.Frontiers in immunology · 2026Review
- Engineering strategies to address immune and delivery barriers in pancreatic ductal adenocarcinoma: a barrier-matched translational framework.Frontiers in immunology · 2026Review
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) is characterized by a profoundly immunosuppressive tumor microenvironment, which features a dense desmoplastic stroma enriched with cancer-associated fibroblasts (CAFs) that collectively impede the efficacy of immunotherapies. Although oncolytic viruses (OVs) have demonstrated promising potential in eliciting antitumor immunity, the mechanisms by which stromal components modulate OV efficacy remain poorly understood.
methodsTo investigate the interplay between immune and stromal components in PDAC following OV treatment, we employed murine and patient-derived tumor models. We characterized immune cell populations using single-cell RNA sequencing and flow cytometry. Functional studies included the engineering of a next-generation oncolytic herpes simplex virus expressing FLT3 ligand, OX40 ligand, and interleukin-12 (IL-12), combined with CD40 agonist antibodies to restore dendritic cell (DC) function and enhance T-cell responses.
resultsWe identified a novel immunosuppressive circuit wherein monocytes, sensing damage-associated molecular patterns and pathogen-associated molecular patterns from OV-infected tumor cells, secrete interleukin-1β. This, in turn, triggers IL-6 production by CAFs, creating an IL-6-rich milieu that impairs DC maturation and co-stimulatory signaling, thereby attenuating T cell-mediated antitumor immunity and restricting OV therapeutic efficacy. Importantly, combination therapy with the engineered OV and CD40 agonist antibodies restored DC functionality and elicited robust tumor-specific T-cell responses in both murine and patient-derived models.
conclusionOur findings reveal a previously unrecognized monocyte-CAF-DC axis that mediates resistance to OV therapy through IL-1β and IL-6-driven suppression of DC function in PDAC. This study provides a mechanistically informed and translationally promising approach to overcome stromal immune suppression, restore effective antitumor immunity, and improve therapeutic outcomes for patients with PDAC.
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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 OpenQuestion graph.