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. 2022 Apr 13;10:20. doi: 10.1186/s40364-022-00373-5

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© The Author(s) 2022

Open AccessThis 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. 3 — Mechanism of action of interruption of the CD47/SIRPα axis. Three mechanisms can be used to inhibit the CD47/SIRPα interaction. Phagocytosis (the most important mechanism of action): blocks the CD47/SIRPα interaction to remove inhibitory signals and promote phagocytosis of tumor cells; Antigen presentation: antiCD47 antibody connects tumor cells and SIRPα+ DCs to promote antigen presentation; Apoptosis: some antiCD47 antibodies could induce tumor cell poptosis