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. Author manuscript; available in PMC: 2023 Nov 16.
Published in final edited form as: J Cancer Metastasis Treat. 2023 Apr 4;9:10. doi: 10.20517/2394-4722.2022.92

Figure 1.

Figure 1.

Direct and Indirect effects of OVs at the tumor site. Direct effect[1–5]: infection of cancer cells[1] leads to the recognition of viral genomes by PRRs[2] and subsequent activation of signaling pathways involved in antiviral defense[3,4]; Type-I interferons and proinflammatory cytokines released to the TME together with DAMPS activation of cell death mechanisms[5] serve as attractants and activators of the innate compartment. Indirect effect[6–8]: licensed APCs cross-present TAA to naïve T-cells[8], allowing for the generation of tumor-specific cytotoxic CD8+ T cells. MDSCs: myeloid-derived suppressor cells; TAMs: Tumor-associated Macrophages; T-regs: regulatory T cells; APC: antigen-presenting cell; OVs: Oncolytic viruses; PRRs: Pattern Recognition Receptors; MHC: Mayor Histocompatibility complex; TAA: tumor-associated antigen; NK: natural killer; NKT: Natural Killer T cells; IRF3: interferon regulatory factor 3; TLR: toll-like receptor; CTL: cytotoxic T-lymphocytes; TME: tumor microenvironment.