RV inhibits the immunosuppressive activity of MDSC in a TLR3-dependent manner, despite virus-mediated upregulation of IL-6 and TNF-α that can promote MDSC activity.62 Interestingly infection of MDSC with VSV, to allow for systemic delivery of VSV by harnessing the tumor-localizing properties of MDSC, converted tumor-promoting MDSCs to tumor-suppressive phenotypes and these populations acted synergistically with VSV to eliminated established tumors.63 Strategies to facilitate OV-mediated MDSC reduction in tumors include hydroxyprostaglandin dehydrogenase (HPGD) enzyme arming of VV. This evidence concerns the gene TLR3 and neoplasm.