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. 2023 May 23;21:345. doi: 10.1186/s12967-023-04200-9

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Changes of mitochondrial function in different cells during drug resistance of melanoma TME. Melanoma cells, Tumor-MDSCs, and TAMs can all express PD-L1, which makes CD8⁺ T cells in a resting state. Among them, the expression of PD-L1 in melanoma cells is related to the JAK1/2-STAT pathway involved in mitochondria, while the expression of PD-L1 in TAM may be related to the PI3K γ-NF κ B pathway. When CD8⁺T cells receive dual-signal stimulation from melanoma cells, they can release IFN- γ to participate in immune regulation. After receiving the extracellular carrier (EV) released by melanoma cells, TAMS also releases interferon-γ and IL-6 to inhibit the immune function of T cells. In addition, melanoma cells can inhibit T cell aggregation by producing VEGF and IL-8 through the MAPK pathway, affecting their mitochondria’s function through the PI3K pathway. Tumor-MDSCs: Tumor-associated myeloid-derived suppressor cells; TAM: Tumor-associated macrophages; IFN- γ: Interferon-gamma; VEGF: Vascular endothelial growth factor; IDO-1: Indoleamine 2,3-Dioxygenase-1; EV: Extracellular vesicle