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• W2734345862 abstract "TGFβ secreted by tumor cells and/or tumor infiltrating stromal cells is a key mediator of tumor growth and immune suppression at the tumor site. Nonetheless, clinical trials in cancer patients targeting the TGFβ pathway exhibited at best a modest therapeutic benefit. A likely reason, a common limitation of many cancer drugs, is that the physiologic roles of TGFβ in tissue homeostasis, angiogenesis, and immune regulation precluded the dose escalation necessary to achieve a profound clinical response. Murine studies have suggested that countering immune suppressive effects of TGFβ may be sufficient to inhibit tumor growth. Here we describe an approach to render vaccine-activated CD8+ T cells transiently resistant to TGFβ inhibition using an siRNA against Smad4 to inhibit a key step in the canonical TGFβ signaling pathway. The siRNA was targeted to vaccine activated CD8+ T cells in the mouse by conjugation to a 4-1BB binding oligonucleotide (ODN) aptamer ligand (4-1BB-Smad4 conjugate). In vitro the 4-1BB-Smad4 conjugate rendered T cells partially resistant to TGFβ inhibition, and treatment of tumor bearing mice with systemically administered 4-1BB-Smad4 conjugate enhanced vaccine- and irradiation-induced antitumor immunity. Limiting the inhibitory effects of TGFβ to tumor-specific T cells will not interfere with its multiple physiologic roles and hence reduce the risk of toxicity." @default.
• W2734345862 created "2017-07-21" @default.
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• W2734345862 date "2018-02-15" @default.
• W2734345862 modified "2023-10-08" @default.
• W2734345862 title "Potentiating tumor immunity using aptamer-targeted RNAi to render CD8⁺ T cells resistant to TGFβ inhibition" @default.
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• W2734345862 doi "https://doi.org/10.1080/2162402x.2017.1349588" @default.
• W2734345862 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5889204" @default.
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• W2734345862 hasPublicationYear "2018" @default.
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