Inflammasomes have emerged as context-dependent regulators of inflammation and protective immunity in vertebrates. Depending on the cell type and stimulus, inflammasome activities lead to interleukin (IL)-1 release from living (hyperactive) or dead (pyroptotic) cells. Herein, we review the mechanisms by which inflammasomes can impact CD8⁺ T cell-mediated antitumor immunity. We describe recent work demonstrating the differential impact of pyroptosis in cancer cells and dendritic cells (DCs) on antitumor immunity. We further highlight the surprising ability of inflammasomes within hyperactive DCs to facilitate the use of tumor lysates as immunogens, promoting CD8⁺ T cell-mediated antitumor responses. These context-dependent roles of inflammasomes in living and dead cells offer much opportunity for future research and should inform discussions of next-generation immunotherapy development.

炎症小体已成为脊椎动物炎症和保护性免疫的上下文依赖性调节剂。根据细胞类型和刺激，炎性小体活动会导致白细胞介素 (IL)-1 从活（过度活跃）或死（焦亡）细胞中释放。在此，我们回顾了炎症小体影响 CD8 ⁺ T 细胞介导的抗肿瘤免疫的机制。我们描述了最近的工作，证明了癌细胞和树突状细胞 (DC) 中细胞焦亡对抗肿瘤免疫的不同影响。我们进一步强调了过度活跃的 DC 中炎性体的惊人能力，以促进使用肿瘤裂解物作为免疫原，促进 CD8 ⁺T细胞介导的抗肿瘤反应。炎症小体在活细胞和死细胞中的这些上下文相关作用为未来的研究提供了很多机会，并应该为下一代免疫疗法的讨论提供信息。