Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile
Highlights • RIG-I activity regulates biogenesis and function of tumor cell-derived EVs • Cancer-intrinsic RIG-I signaling governs the composition of the EV RNA cargo • Immunostimulatory EVs trigger T cell-based antitumor immunity in mice and humans • EV and RIG-I gene signatures in melanomas correlate with response to immunotherapy Summary Tumor-derived extracellular vesicles (EVs) have been associated with immune evasion and tumor progression.
Highlights • RIG-I activity regulates biogenesis and function of tumor cell-derived EVs • Cancer-intrinsic RIG-I signaling governs the composition of the EV RNA cargo • Immunostimulatory EVs trigger T cell-based antitumor immunity in mice and humans • EV and RIG-I gene signatures in melanomas correlate with response to immunotherapy Summary Tumor-derived extracellular vesicles (EVs) have been associated with immune evasion and tumor progression.
Priming responses to checkpoint blockade Although activation of intracellular DNA sensing has been proposed as a means to promote antitumor immunity, molecules that regulate sensing of intracellular RNAs have received considerably less attention in this setting. Here, Heidegger et al. report that expression of RNA sensor RIG-I in tumor cells plays a vital role in promoting responsiveness to anti–CTLA-4 therapy in mouse models of cancer.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
