Figure 2.

(1) Oncolytic viruses (OV) infect glioma cells, initiating the process of immunogenic cell death (ICD). Dying glioma cells release damage associated molecular patterns (DAMP) and type I interferons, molecules that stimulate the host’s immune response. Following the virus-mediated lysis of the cell, oncolytic virus is released into the surrounding tissue and can infect adjacent glioma cells. (2) Tumor-associated antigens (TAA) recruit immature antigen-presenting cells (APC) to the tumor. (3) APC become activated following antigen-uptake and begin interacting with DAMP via pattern recognition receptors (toll-like receptors (TLR) and nod-like receptors (NLR)). (4) Following this interaction, immature antigen-capturing APC become mature APC, which are able to form and transport peptide-loaded MHC complexes to the cell surface. (5) Mature APC migrate to a regional lymph node where they prime naïve T cells. This is followed by clonal expansion and then release of cytotoxic CD8⁺ T lymphocytes (CTL). (6) These tumor specific CTL are attracted to the tumor by cytokines released from dying glioma cells. Natural killer (NK) cells, part of the innate immune system, are attracted to the tumor by chemokine. Altogether, this generates an anti-tumor immune response. (7) Continuous exposure of TAA to CTL promotes immunological memory, generating memory CD8⁺ T cells.