Senescent cells (SCs) arise from normal cells in multiple organs due to inflammatory, metabolic, DNA damage, or tissue damage signals. SCs are non-proliferating but metabolically active cells that can secrete a range of pro-inflammatory and proteolytic factors as part of the senescence-associated secretory phenotype (SASP). Senescent cell anti-apoptotic pathways (SCAPs) protect SCs from their own pro-apoptotic SASP. SCs can chemo-attract immune cells and are usually cleared by these immune cells. During aging and in multiple chronic diseases, SCs can accumulate in dysfunctional tissues. SCs can impede innate and adaptive immune responses. Whether immune system loss of capacity to clear SCs promotes immune system dysfunction, or conversely whether immune dysfunction permits SC accumulation, are important issues that are not yet fully resolved. SCs may be able to assume distinct states that interact differentially with immune cells, thereby promoting or inhibiting SC clearance, establishing a chronically pro-senescent and pro-inflammatory environment, leading to modulation of the SASP by the immune cells recruited and activated by the SASP. Therapies that enhance immune cell-mediated clearance of SCs could provide a lever for reducing SC burden. Such therapies could include vaccines, small molecule immunomodulators, or other approaches. Senolytics, drugs that selectively eliminate SCs by transiently disabling their SCAPs, may prove to alleviate immune dysfunction in older individuals and thereby accelerate immune-mediated clearance of SCs. The more that can be understood about the interplay between SCs and the immune system, the faster new interventions may be developed to delay, prevent, or treat age-related dysfunction and the multiple senescence-associated chronic diseases and disorders.

衰老细胞 (SC) 由于炎症、代谢、DNA 损伤或组织损伤信号而由多个器官中的正常细胞产生。SC 是非增殖但代谢活跃的细胞，可以分泌一系列促炎和蛋白水解因子，作为衰老相关分泌表型 (SASP) 的一部分。衰老细胞抗凋亡途径 (SCAP) 保护 SC 免受自身促凋亡 SASP 的影响。SC 可以化学吸引免疫细胞，并且通常被这些免疫细胞清除。在衰老过程中和多种慢性疾病中，SCs 会积聚在功能失调的组织中。SC 可以阻碍先天性和适应性免疫反应。免疫系统清除SCs能力的丧失是否会促进免疫系统功能障碍，或者相反，免疫功能障碍是否会导致SCs积累，是尚未完全解决的重要问题。SC 可能能够呈现与免疫细胞相互作用的不同状态，从而促进或抑制 SC 清除，建立长期促衰老和促炎症环境，导致 SASP 招募和激活的免疫细胞对 SASP 进行调节。增强免疫细胞介导的干细胞清除的疗法可以为减轻干细胞负担提供杠杆。此类疗法可能包括疫苗、小分子免疫调节剂或其他方法。Senolytics 是一种通过暂时禁用 SCAP 来选择性消除 SC 的药物，可能会减轻老年人的免疫功能障碍，从而加速免疫介导的 SC 清除。对 SC 和免疫系统之间的相互作用了解得越多，就越能更快地开发出新的干预措施来延迟、预防或治疗与年龄相关的功能障碍以及多种与衰老相关的慢性疾病和病症。