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. 2022 Jan 15;10:4. doi: 10.1186/s40364-021-00346-0

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© The Author(s) 2021

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. 1 — The role of phosphatidylserine in immunity and blood coagulation. In the blood coagulation system, (1) PtdSer exposed on activated platelets can bind to the Tenase complex and Prothrombinase complex to promote the generation of thrombin. To form a clot at the injured site to achieve a hemostatic effect, thrombin activates downstream signaling pathways [28–32]. (2) PtdSer exposed on activated platelets can bridge with TAM receptors through the GAS6 ligand to promote platelet aggregation to maintain thrombosis and platelet stability [33]. (3) The thrombin generated through (1) can also bind to thrombomodulin to catalyze the production of Activated Protein C from Protein C. Subsequently, they inactivate Tenase complex and Prothrombinase complex, inhibiting blood coagulation. During this process, PROS1 support the anticoagulant activity of Activated Protein C [28–32]; In the immune system, (4) PtdSer exposed on the surface of apoptotic cells can be recognized and bound by PtdSer receptors, such as TIM, TAM, on the surface of phagocytes, leading to phagocytosis of apoptotic cells [19, 34, 35]. (5) The PtdSer exposed on the surface of some viruses, such as the Ebola Virus, Dengue Virus, can binds to PtdSer receptors on immune cells (i.e., TIM, TAM, etc.), allowing the virus to invade hosts [9–15]. (6) PtdSer exposed on tumor or cancer cells can also bind to PtdSer receptors (e.g., TIM, TAM) expressed on immune cells to trigger immunosuppressive pathways and ultimately promote immune escape [19–22]