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. 2022 Apr 16;13(4):355. doi: 10.1038/s41419-022-04775-z

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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. 6 — In dealing with ferroptotic cells, TLR2 on macrophages identifies and binds to SAPE-OOH on the surface of ferroptotic cells to enhance engulfment. HMGB1 released by dying cells can interact with AGRE on macrophages in order to mediate inflammation reactions in macrophages. Some molecules like CCL2 or CCL7 can initiate the recruitment and chemotaxis of macrophages for intensity of immune reactions.