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. 2022 Oct 11;8:416. doi: 10.1038/s41420-022-01206-y

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© The Author(s) 2022

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 — The classical effect of TTFields is mitosis inhibitions and formation of apocyte. A TTFields induces various mode of tumor cell death, including apoptosis, autophagy, pyroptosis, immunogenic death, necrosis, necroptosis, and cell cycle arrest. Meanwhile, TTFields affects the integrity of membrane and the blood-brain barrier, increasing permeability of tumor cell. B TTFields induces activation of dendritic cell, RAW264.7. In addition, TTFields leads to T cell infiltration and CD45 + leukocyte enrichment. Meanwhile, T1IRG-expressing monocyte, NK cell and immune checkpoints are elevated after TTFields treatment.