Figure 2.

Schematic presentation of virus initiated antitumor T-cell response. Locally administered replication-competent virus activates the innate immune system via pathogen-associated molecular pattern (PAMP) and danger-associated molecular pattern (DAMP) receptors. Virus replication causes an immunogenic cancer cell death leading to exposure of calreticulin A on the outer surface of tumor cells, and release of ATP, HMGB1, and tumor antigens from dying cancer cells. All these signals increase the activity of antigen-presenting cells (APCs), which take up and process tumor antigens. Maturation of APCs and local immunostimulation can be further enhanced by virus-coded transgene. APCs present antigens to T-cells in the draining lymph node leading to systemic T-cell attack against tumors.