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. 2021 Oct 1;12(10):894. doi: 10.1038/s41419-021-04171-z

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — In DDR, P53 activated the tumor suppressor-activated pathway 6 (TSAP6) to increase the secretion of exosomes. Additionally, mutant P53 can selectively increase the release of miR-1246-enriched exosomes. And these miR-1246-enriched exosomes contribute to anti-inflammatory immunosuppression by inducing high levels of TGF-β activity. As a stress reaction, senescence enhanced the biosynthesis of exosome-like vesicles, and further several highly reactive agents were liberated via EVs. When cellular DNA damages appeared, EVs secretion contributed to maintain intercellular homeostasis via excreting the harmful cytoplasmic DNA fragments. dsDNA and mtDNA can upregulate the expressions of type I IFNs by activating cGAS/STING pathway. Additionally, exoDNA can be absorbed by innate immune cells in the intestine to stimulate the activation of the inflammasome and then enhance the secretion of IL-18 and IL-1β. RN7SL1 activates RIG-I in immune cells to accelerate the tumor growth. Importantly, dsRNA is deemed as a contributor of anti-cancer immunity since it recruits T cells into the tumor microenvironment through increasing the secretion of TLR3-dependent cytokines including type I IFN and CXCL10.