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. 2022 Oct 26;8:427. doi: 10.1038/s41420-022-01218-8

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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. 5 — Ferroptosis induction facilitates MCH-1 expression, release of DAMPS and IFNγ, which in turn activate immune cell activity including T cells and macrophages. In addition, the release of IFNγ from T cells inhibits Xc (-) system (SLC7A11/SLC3A2), leading to increased ferroptosis sensitivity. Ferroptosis resistance by GPX4 in Treg cells causes immune tolerance. As an eat-me signal, SAPE-OOH is distributed on ferroptotic cancer cells, which is recognized by TLR2 on macrophages leading to increased phagocytosis. Although combined immune checkpoint inhibitors with ferroptosis inducers could effectively enhance antitumor immunotherapy, induction of ferroptosis could impair T cell survival by ferroptosis. Therefore, a rational combined therapy is essential.