因肿瘤微环境的不可穿透性，使免疫疗法的功效受到限制。许多肿瘤的微环境是免疫特权的，从而使它们能够逃避宿主的免疫监视。这种情况发生的机制之一是通过CD47的过度表达，这是一种“别吃我”的蛋白质，可以与髓系细胞上的SIRPα相互作用，抑制它们的吞噬作用。近年来，许多研究都集中在CD47-SIRPα依赖性免疫疗法上，以激发吞噬细胞和肿瘤之间的“寻找并吃掉”的相互作用。因此，在本篇综述中，我们重点介绍了CD47-SIRPα级联反应的基本分子特性和机制。此外，我们还讨论了与CD47-SIRPα基于免疫疗法相关的主要挑战和潜在解决方案。 版权©2023 Elsevier B.V.版权所有。

The efficacy of immunotherapies is limited due to the impenetrable nature of the tumor microenvironment (TME). The TME of many tumors is immune-privileged, thus allowing them to evade host immunosurveillance. One mechanism through which this occurs is via the overexpression of CD47, a 'don't eat me' protein that can interact with SIRPα on myeloid cells to suppress their phagocytic action. In recent times, many studies are focusing on CD47-SIRPα-dependent immunotherapies to incite a 'seek and eat' interaction between phagocytes and tumors. Thus, in this review, we highlight the basic molecular properties and mechanisms of CD47-SIRPα cascade. In addition, we discuss the major challenges and potential remedies associated with CD47-SIRPα-based immunotherapies.Copyright © 2023 Elsevier B.V. All rights reserved.