巨噬细胞介导的程序性细胞去除（PrCR）对于识别和消除维持组织稳态的不需要的细胞至关重要。 PrCR 的功效取决于促吞噬细胞“吃我”信号和抗吞噬细胞“别吃我”信号之间的平衡。近年来，越来越多的研究表明肿瘤的发生和进展与PrCR密切相关。在肿瘤微环境中，“吃我”信号激活的PrCR被CD47/SIRPα的“别吃我”信号抵消，导致肿瘤免疫逃逸。因此，针对令人兴奋的“吃我”信号，同时抑制“别吃我”信号并最终诱导巨噬细胞产生有效的PrCR将是一种非常有吸引力的抗肿瘤策略。在此，我们全面综述PrCR激活信号分子（CRT、PS、Annexin1、SLAMF7）和PrCR抑制信号分子（CD47/SIRPα、MHC-I/LILRB1、CD24/Siglec-10、SLAMF3、SLAMF4、PD）的功能。 -1/PD-L1、CD31、GD2、VCAM1)，这些分子之间的相互作用以及 Warburg 效应。此外，我们重点介绍了通过刺激或抑制 PrCR 影响免疫系统功能的分子调节机制。最后，我们回顾了通过激活 PrCR 进行肿瘤治疗的研究进展，并讨论了挑战和潜在的解决方案，为针对 PrCR 的肿瘤治疗策略铺平道路。版权所有 © 2024。由 Elsevier B.V. 出版。

Macrophage-mediated programmed cell removal (PrCR) is crucial for the identification and elimination of needless cells that maintain tissue homeostasis. The efficacy of PrCR depends on the balance between pro-phagocytic "eat me" signals and anti-phagocytic "don't eat me" signals. Recently, a growing number of studies have shown that tumourigenesis and progression are closely associated with PrCR. In the tumour microenvironment, PrCR activated by the "eat me" signal is counterbalanced by the "don't eat me" signal of CD47/SIRPα, resulting in tumour immune escape. Therefore, targeting exciting "eat me" signalling while simultaneously suppressing "don't eat me" signalling and eventually inducing macrophages to produce effective PrCR will be a very attractive antitumour strategy. Here, we comprehensively review the functions of PrCR-activating signal molecules (CRT, PS, Annexin1, SLAMF7) and PrCR-inhibiting signal molecules (CD47/SIRPα, MHC-I/LILRB1, CD24/Siglec-10, SLAMF3, SLAMF4, PD-1/PD-L1, CD31, GD2, VCAM1), the interactions between these molecules, and Warburg effect. In addition, we highlight the molecular regulatory mechanisms that affect immune system function by exciting or suppressing PrCR. Finally, we review the research advances in tumour therapy by activating PrCR and discuss the challenges and potential solutions to smooth the way for tumour treatment strategies that target PrCR.Copyright © 2024. Published by Elsevier B.V.