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. 2023 Aug 31;11(8):e007253. doi: 10.1136/jitc-2023-007253

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© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Working model for VBL-mediated antitumor immune response. VBL phosphorylates and activates the transcription factor NF-κB in TAMs, upregulating cyba which encodes p22^phox protein expression. Cytosolic ROS and MitoROS levels were increased by p22^phox -catalyzed synthesis. ROS further facilitated the entry of transcription factor TFEB into the nucleus, accelerating lysosome biogenesis and activation, and thus endowing TAMs with a higher phagocytic capacity. ROS also repolarized TAMs into the M1-like phenotype and abolished their suppressive activity on CD8⁺ T cells. This graph model was created with biorender.com. ROS, reactive oxygen species; TAMs, tumor-associated macrophage; VBL, vinblastine.