fig1

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.