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. Author manuscript; available in PMC: 2020 Jan 8.
Published in final edited form as: Immunity. 2018 Mar 20;48(3):417–433. doi: 10.1016/j.immuni.2018.03.007

Figure 3: Activation of pattern recognition receptors by conventional and targeted therapies can promote innate immune signaling.

Figure 3:

Radiation and genotoxic agents can lead to activation of the cGAS/STING pathway intrinsically in tumor cells as well as in dendritic cells. Altered cell cycle machinery in tumor cells allows progression through mitosis despite DNA damage, leading to the accumulation of cGAS positive nuclei. Epigenetic therapy with DNA methyltransferase inhibitors (DNMTi) and histone deacetylase inhibitors (HDACi) can derepress endogenous retroviruses (ERVs) in a mechanism termed virus mimicry. Targeted therapies such as CDK4/6 inhibitors have also been shown to promote interferon signaling through this mechanism. Changes in RNA binding proteins can lead to unshielding of dsRNA, allowing RIG-I activation. Chemotherapy, such as adriamycin, can activate TLR3 signaling to promote anti-tumor immune responses. Oncolytic viruses have multi-faceted effects on innate immune signaling through activation of PRR and promotion of immunogenic cell death (ICD). Direct STING and TLR agonists are also being developed.