2021
DOI: 10.1016/j.virusres.2021.198440
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Oncolytic reovirus induces ovarian cancer cell apoptosis in a TLR3-dependent manner

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Cited by 9 publications
(4 citation statements)
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“…Targeting TLRs can have anti-tumor activity by promoting antigen presentation and activating innate and adaptive immunity (213,214). All three, RIG-I, MDA5 and TLRs can be activated by some OVs, providing the possibility for combining agonist of these receptors with OVs (215)(216)(217)(218)(219). However, the combination therapy has to avoid sensitizing the patient to a cytokine shock-like response induced by IV delivery of OVs (220).…”
Section: Finding Suitable Markers For Evaluating the Effectiveness Of Therapymentioning
confidence: 99%
“…Targeting TLRs can have anti-tumor activity by promoting antigen presentation and activating innate and adaptive immunity (213,214). All three, RIG-I, MDA5 and TLRs can be activated by some OVs, providing the possibility for combining agonist of these receptors with OVs (215)(216)(217)(218)(219). However, the combination therapy has to avoid sensitizing the patient to a cytokine shock-like response induced by IV delivery of OVs (220).…”
Section: Finding Suitable Markers For Evaluating the Effectiveness Of Therapymentioning
confidence: 99%
“…12 Moreover, OVs can activate various forms of immunogenic cell death (ICD), including immunogenic apoptosis, necroptosis and pyroptosis, by inducing endoplasmic reticulum (ER) stress, 77,78 leading to the release of hallmark immunostimulatory damage-associated molecular patterns (DAMPs), such as ATP, high mobility group box 1 protein (HMGB1), heat shock protein, ectocalreticulin and proinflammatory cytokines. 79,80 These PAMPs and DAMPs are sensed by pattern recognition receptors (PRRs), such as stimulator of IFN genes (STING), Toll-like receptor (TLR) adaptor molecule 1 and TLR3 on immune cells, [81][82][83] establishing a proinflammatory microenvironment by stimulating the production of proinflammatory cytokines, such as type I IFNs, interleukin (IL)-1β, IL-6, IL-12, TNF-α, GM-CSF, and chemokines, such as CCL2, CCL3, CCL5, and CXCL10, leading to the transformation of immunologically "cold" tumors into "hot" tumors. 71 First, locally secreted chemokines, such as CCL3 and CXCL10, recruit the first cell responders, such as neutrophils and macrophages, to the site of infection, 84 and these cytokines are involved in the induction of effective antitumor responses.…”
Section: Mechanism Of Ov Actionmentioning
confidence: 99%
“…I IFN, interleukin (IL)−1β, IL-6, IL-12, TNF-α, granulocyte macrophage colony-stimulating factor (GM-CSF). [44][45][46] In addition, chemokines, such as CCL2, CCL3, CCL5, and CXCL10. [47][48][49] It is known that cytokines attract neutrophils and macrophages, and these cytokines activate innate immune cells like natural killer (NK) cells and DCs, further stimulating the production of IFNs, TNF-α, IL-6, IL-12, and chemokines, ultimately turning "cold" tumors into "hot" ones, 50 as shown in Figure 2.…”
Section: Mechanism Of Action Of Ovsmentioning
confidence: 99%
“…OVs induce immunogenic cell death of tumor cells to release a variety of molecules, including pathogen‐associated molecular pattern molecules (PAMPs), damage‐associated molecular pattern molecules (DAMPs), tumor‐associated antigens (TAAs), and tumor‐associated neoantigens 43 . Tumor cells and immune cells activate the expression of inflammatory factors through PAMPs/DAMPs mode, such as type I IFN, interleukin (IL)−1β, IL‐6, IL‐12, TNF‐α, granulocyte macrophage colony‐stimulating factor (GM‐CSF) 44–46 . In addition, chemokines, such as CCL2, CCL3, CCL5, and CXCL10 47–49 .…”
Section: Mechanism Of Action Of Ovsmentioning
confidence: 99%