期刊
ONCOIMMUNOLOGY
卷 8, 期 4, 页码 -出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/2162402X.2019.1570779
关键词
Immunogenic cell death; pattern recognition receptors; nucleic acid receptors; RIG-I; anticancer vaccine; dendritic cells; tumor immunotherapy; personalized medicine
资金
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [360372040 - SFB 1335]
- Deutsche Forschungsgemeinschaft [PO 1575/3-1]
- Deutsche Krebshilfe [111620]
- Else Kroner-Fresenius-Stiftung [2015_A06, 2012_A61]
- European Hematology Association
- DKMS [Mechtild Harf Research Grant]
- Carl Maximilian and Carl Manfred Bayer-Foundation
- Else Kroner-Fresenius-Stiftung [Forschungskolleg TUM]
Resistance to cell death and evasion of immunosurveillance are major causes of cancer persistence and progression. Tumor cell-intrinsic activation of the RNA receptor retinoic acid-inducible gene-I (RIG-I) can trigger an immunogenic form of programmed tumor cell death, but its impact on antitumor responses remains largely unexplored. We show that activation of intrinsic RIG-I signaling induces melanoma cell death that enforces cross-presentation of tumor-associated antigens by bystander dendritic cells. This results in systemic expansion and activation of tumor-antigen specific T cells in vivo with subsequent regression of pre-established melanoma. These processes were dependent on the signaling hub MAVS and type I interferon (IFN-I) signaling in the host cell. Using melanoma cells deficient for the transcription factors IRF3 and IRF7, we demonstrate that RIG-I-activated tumor cells used as a vaccine are a relevant source of IFN-I during T cell cross-priming in vivo. Thus, our findings may facilitate translational development of personalized anticancer vaccines.
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