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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. 1 — The autophagy-associated complex (ATG5–ATG16) translocalized to MVBs and dissociated vacuolar proton pumps (V-ATPase) from MVBs, in which the acidification of the MVBs lumen was inhibited. Ultimately, the secretion of EVs augmented via MVBs–plasma membrane (PM) fusion. In addition, amphisomes were formed by the fusion of autophagosomes and MVBs, which accelerated the EVs release controlled by RAB8A and RAB27A. Immunoregulatory factors including ANXA2 and ATP were contained in EVs, ANXA2 can induce an increased secretion of TNFα and IL6 by activating the STAT3, p38, and NF-κB pathways in macrophages. In addition, ANXA2 promotes tPA-dependent angiogenesis. ATP can promote the differentiation of CD11b⁺CD11c⁺Ly6C^high cells into mature DCs by binding with purinergic receptor P2Y2, and upregulate the IL-1β production through NLRP3 inflammasome, ultimately stimulating the activation of anti-tumor CTL responses. However, adenosine can be converted from ATP hydrolyzed by CD39 and CD73, further inhibiting T-cell activation through binding with the adenosine A(2 A) receptor.