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. 2023 Mar 1;11(3):e005430. doi: 10.1136/jitc-2022-005430

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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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Schematic diagram of the mechanistic findings. Tfam deficiency in DCs resulted in mitochondrial metabolism abnormalities (number 1), then the cGAS-STING pathway actived (number 2), subsequently enhanced the immunity of DCs and T cells and resultantly inhibiting lung metastases of the tumor by remodeling the tumor microenvironment (number 3). Furthermore, spleen T lymphocytes of immunized Tfam^-/- mice displayed stronger antitumor immunity when adoptively transferred into tumor-bearing wild type mice. DCs, dendritic cells.