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Tumor cell-intrinsic RIG-I signaling governs synergistic effects of immunogenic cancer therapies and checkpoint inhibitors in mice.

Abstract
Immunogenic cancer therapies, including radiation and hypomethylating agents, such as 5-azacytidine, rely on tumor cell-intrinsic activation of the RNA receptor RIG-I for their synergism with immune checkpoint inhibitors. Possible RIG-I ligands are small nuclear RNA (snRNA) and endogenous retroviral elements (ERV) leaking from the nucleus during programmed cell death.
AuthorsHendrik Poeck, Alexander Wintges, Sarah Dahl, Florian Bassermann, Tobias Haas, Simon Heidegger
JournalEuropean journal of immunology (Eur J Immunol) Vol. 51 Issue 6 Pg. 1531-1534 (06 2021) ISSN: 1521-4141 [Electronic] Germany
PMID33733474 (Publication Type: Letter, Research Support, Non-U.S. Gov't)
Copyright© 2021 The Authors. European Journal of Immunology published by Wiley-VCH GmbH.
Chemical References
  • Immune Checkpoint Inhibitors
  • Receptors, Cell Surface
  • Robo3 protein, mouse
  • Azacitidine
Topics
  • Animals
  • Azacitidine (therapeutic use)
  • Chemoradiotherapy
  • Disease Models, Animal
  • Drug Synergism
  • Humans
  • Immune Checkpoint Inhibitors (therapeutic use)
  • Immunotherapy (methods)
  • Melanoma (immunology, therapy)
  • Melanoma, Experimental
  • Mice
  • Mice, Inbred C57BL
  • Receptors, Cell Surface (genetics, metabolism)
  • Signal Transduction
  • Treatment Outcome

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