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. 2020 Jun 25;11(6):485. doi: 10.1038/s41419-020-2696-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Oncolytic viruses can be transduced to deliver antitumor agents, such as TRAIL, interleukins (IL-12, IL-4, and IL-15), immune checkpoint inhibitors (anti-PD-1 antibody), immune-enhancing stimulators (OX40L and GM-CSF), tumor suppressors (PTEN and P53), E-cad and Flt3L, and are systemically administered to GBM sites. Afterward, OVs bind to certain receptors to infect and enter tumor cells, resulting in tumor lysis. OVs that are armed with immune factors can enhance antiglioma efficacy by recruiting immune cells, which include T cells, NK cells, and macrophages, to the GBM sites. These activated immune cells can secrete certain antitumor cytokines, including IFN-γ, IFN-β, TNF-α, TNF-β, IL-2, and IL-6, which ultimately induce tumor cell apoptosis by specific signaling pathways. In summary, OVs expressing immunomodulatory transgenes effectively lead to tumor recession by the combination of virotherapy and immunotherapy.