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From the foregoing discussion, it is clear that suppression of host cell protein synthesis in virus infected cells has the potential to negatively impact the expression and presentation of tumor associated antigens. Russell and Barber, Mayo Clinic and University of Miami have a financial interest in Vyriad, an oncolytic virotherapy company. The ratio of viral to tumor antigens delivered to phagocytosing APCs is therefore predicted to become progressively more favorable to the tumor antigens as the infection progresses. The body has evolved processes to efficiently eliminate apoptotic cells via phagocytosis while at the same time ensuring that there are no inflammatory counter reactions Nagata and Tanaka, 2017. See other articles in PMC that cite the published article. Innate immune agonists may also be useful in helping to boost OV-mediated cross priming. Such STING agonists may also help overcome checkpoint inhibition, by increasing the production of anti-tumor T lymphocytes Corrales et al.

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Thus, as discussed below, in oncolytic virotherapy, tumor cell PAMPs may be more important drivers of adjuvanticity and effective antigen presenting cell APC engagement than the mode of cell death. Also, epitope interference in models of virus infection and tissue rejection is readily overcome by increasing the number of antigen-bearing APCs or the precursor frequency of T cells reacting with the nondominant antigen Kedl et al. Below we discuss our current understanding of the impact of OV infection both on adjuvanticity and antigenicity of dead or dying tumor cells and how this primes and amplifies the available pool of tumor-killing TAA-reactive CTLs. Innate immune DNA sensing pathways: Engineering OVs for Cancer Immunotherapy Aside from their selective intratumoral propagation and inflammatory tumor cell killing, OVs can be engineered to further modulate their impact on tumor-immune system interactions Elsedawy and Russell, 2013.

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After phagocytosis, tumor cell nucleic acid is proficiently digested by DNases before it can robustly activate innate immune pathways and trigger cytokine production, including type I interferons which are required to stimulate cross-priming events and facilitate anti-tumor T cell activity Nagata and Tanaka, 2017 ; Schiavoni et al. Aside from the progressive attenuation of viral antigen expression in phagocytosed OV-infected tumor cells, additional factors may disfavor the suppression of TAA reactive CTL during an OV infection. Herpes simplex virus inhibits host cell splicing, and regulatory protein ICP27 is required for this effect. But besøk siden are only temporary holding measures that serve to slow, but not stop, the crescendo of innate and adaptive host immune responses. Oncolytic viruses-immunotherapeutics on the rise. An alternative OV engineering strategy has been to inactivate the molecular mechanisms used by certain viruses to suppress or evade immune detection. Please review our privacy policy.

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