Department of Biochemistry, School of Medicine, University of Costa Rica, 11501-2060 San José, Costa Rica; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Parker Institute for Cancer Immunotherapy, San Francisco, CA, USA.
Trends Immunol. 2021 Nov;42(11):975-993. doi: 10.1016/j.it.2021.09.002. Epub 2021 Oct 2.
The cancer-immunity cycle (CIC) comprises a series of events that are required for immune-mediated control of tumor growth. Interruption of one or more steps of the CIC enables tumors to evade immunosurveillance. However, attempts to restore antitumor immunity by reactivating the CIC have had limited success thus far. Recently, numerous studies have implicated metabolic reprogramming of tumor and immune cells within the tumor microenvironment (TME) as key contributors to immune evasion. In this opinion, we propose that alterations in cellular metabolism during tumorigenesis promote both initiation and disruption of the CIC. We also provide a rationale for metabolically targeting the TME, which may assist in improving tumor responsiveness to chimeric antigen receptor (CAR)-transduced T cells or immune checkpoint blockade (ICB) therapies.
癌症免疫循环（CIC）包括一系列事件，这些事件是免疫介导控制肿瘤生长所必需的。CIC 的一个或多个步骤的中断使肿瘤能够逃避免疫监视。然而，迄今为止，通过重新激活 CIC 来恢复抗肿瘤免疫的尝试收效甚微。最近，许多研究表明，肿瘤和肿瘤微环境（TME）中的免疫细胞的代谢重编程是免疫逃逸的关键因素。在本观点中，我们提出肿瘤发生过程中细胞代谢的改变促进了 CIC 的启动和中断。我们还为代谢靶向 TME 提供了一个基本原理，这可能有助于提高肿瘤对嵌合抗原受体（CAR）转导 T 细胞或免疫检查点阻断（ICB）治疗的反应性。
