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. 2023 Mar 7;8:104. doi: 10.1038/s41392-023-01365-z

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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 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. 4 — The “eat me” signals calreticulin and SLAMF7. a Stressed and dying tumor cells expose calreticulin on the surface of the cell from ER, and cell surface calreticulin binds to LRP1 on the phagocyte. LRP1 may recruit GULP1, an adapter protein LRP1 for regulating further phagocytic processes. b SLAMF7 on macrophage binds to MAC-1 on the macrophage, and MAC-1 interacts with FCRγ and DAP12 recruiting Src family Syk, and Btk kinases and promoting phagocytosis. SLAMF7 on macrophages combining with SIRPα on macrophage may affect the CD47-SIRPα axis, SLAMF7 in hematological cancers binds SLAMF7 on phagocytes and is necessary for phagocytosis