慢性炎症已被认为是典型的癌症标志。它是由细胞因子精心策划的，细胞因子是肿瘤微环境 (TME) 的主要调节因子，因为它们代表癌细胞、肿瘤基质和免疫系统之间的主要沟通桥梁。白细胞介素 (IL)-6 是炎症与癌症之间联系的关键细胞因子。 IL-6 家族的许多细胞因子，包括 IL-6、制瘤素 M、白血病抑制因子、IL-11、IL-27、IL-31、睫状神经营养因子、心肌营养素 1 和心肌营养素样细胞因子 1，具有已被证明可以通过调节 TME 来引发肿瘤促进作用，使它们成为癌症治疗中有吸引力的治疗靶点。免疫检查点阻断 (ICB) 免疫疗法的发展从根本上改变了包括黑色素瘤、肺癌和肾癌在内的一些癌症的结果，尽管没有障碍。然而，ICB 对其他实体瘤的疗效有限。最近的报告支持慢性炎症和 IL-6 细胞因子信号转导与免疫疗法的抵抗有关。本综述总结了有关 IL-6 相关细胞因子在调节免疫 TME 和 ICB 反应中的影响的现有临床前和临床数据。此外，还讨论了将 ICB 与针对 IL-6 细胞因子成员的疗法相结合来治疗癌症的潜在临床益处。© 作者（或其雇主）2023。CC BY-NC 允许重复使用。不得商业再利用。请参阅权利和权限。英国医学杂志出版。

Chronic inflammation has been recognized as a canonical cancer hallmark. It is orchestrated by cytokines, which are master regulators of the tumor microenvironment (TME) as they represent the main communication bridge between cancer cells, the tumor stroma, and the immune system. Interleukin (IL)-6 represents a keystone cytokine in the link between inflammation and cancer. Many cytokines from the IL-6 family, which includes IL-6, oncostatin M, leukemia inhibitory factor, IL-11, IL-27, IL-31, ciliary neurotrophic factor, cardiotrophin 1, and cardiotrophin-like cytokine factor 1, have been shown to elicit tumor-promoting roles by modulating the TME, making them attractive therapeutic targets for cancer treatment.The development of immune checkpoint blockade (ICB) immunotherapies has radically changed the outcome of some cancers including melanoma, lung, and renal, although not without hurdles. However, ICB shows limited efficacy in other solid tumors. Recent reports support that chronic inflammation and IL-6 cytokine signaling are involved in resistance to immunotherapy. This review summarizes the available preclinical and clinical data regarding the implication of IL-6-related cytokines in regulating the immune TME and the response to ICB. Moreover, the potential clinical benefit of combining ICB with therapies targeting IL-6 cytokine members for cancer treatment is discussed.© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.