Immune checkpoint blockers improve the overall survival of a limited number of patients among different cancers. Identifying pathways that influence the immunological and clinical response to treatment is critical to improve the therapeutic efficacy and predict clinical responses. Recently, a key role has been assigned to innate immune mechanisms in checkpoint blockade-driven anti-tumor responses. However, inflammatory pathways can both improve and impair anti-tumor immunity. In this review, we discuss how different inflammatory pathways, particularly inflammasome activation, can influence the clinical outcome of immune checkpoint blockers. Inflammasome activation may reinforce anti-tumor immunity by boosting CD8+ T cell priming as well as by enhancing T helper type 17 (Th17) responses. In particular, we focus on the modulation of the cation channel transmembrane protein 176B (TMEM176B) and the ectonucleotidase CD39 as potential targets to unleash inflammasome activation leading to reinforced anti-tumor immunity and improved efficacy of immune checkpoint blockers. Future studies should be aimed at investigating the mechanisms and cell subsets involved in inflammasome-driven anti-tumor responses.

中文翻译：

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炎性体激活在免疫检查点阻滞剂触发的肿瘤免疫中的作用。

免疫检查点阻滞剂可改善不同癌症中有限数量患者的总体生存率。识别影响对治疗的免疫学和临床反应的途径对于提高治疗效果和预测临床反应至关重要。最近，在检查点封锁驱动的抗肿瘤反应中，先天免疫机制被赋予了关键作用。但是，炎性途径可以改善和削弱抗肿瘤免疫力。在这篇综述中，我们讨论了不同的炎症途径，尤其是炎症小体激活如何影响免疫检查点阻滞剂的临床结果。炎性体激活可以通过增强CD8 + T细胞启动以及增强T辅助17型（Th17）应答来增强抗肿瘤免疫力。尤其是，我们专注于调节阳离子通道跨膜蛋白176B（TMEM176B）和外切核苷酸酶CD39作为释放炎症小体激活的潜在靶标，从而导致增强的抗肿瘤免疫力和免疫检查点阻断剂的疗效。未来的研究应旨在研究炎症小体驱动的抗肿瘤反应的机制和细胞亚群。