组织内促炎性衰老细胞的积累是衰老过程和许多与年龄相关的疾病的共同标志。这种修饰被称为衰老相关分泌表型（SASP），并在培养细胞和从衰老组织中分离的细胞中观察到。目前，组织内衰老细胞的积累是否应归因于衰老细胞生成的增加，还是衰老细胞从衰老组织中消除的缺陷，存在争议。新兴研究表明，衰老细胞中多种抑制性免疫检查点配体的表达增加，尤其是程序性细胞死亡蛋白 1 (PD-1) 配体 1 (PD-L1) 蛋白的表达增加。众所周知，PD-L1 配体，尤其是癌细胞的 PD-1 配体，靶向细胞毒性 CD8 T 和自然杀伤 (NK) 细胞的 PD-1 受体，干扰其功能，例如引起其细胞毒性活性下降并促进其耗竭甚至细胞凋亡。衰老细胞中 PD-L1 蛋白水平的增加能够抑制其免疫监视，并抑制细胞毒性 CD8 T 和 NK 细胞对它们的消除。已知衰老细胞表达多种抑制性免疫检查点受体的配体，即 PD-1、LILRB4、NKG2A、TIM-3 和 SIRPα 受体。在这里，我将简要描述这些途径，并检查这些抑制性检查点是否可能参与衰老细胞和年龄相关疾病的免疫逃避。增强的抑制性检查点信号传导可以阻止衰老细胞从组织中消除，从而促进衰老过程，这似乎是合理的。© 2024。作者。

The accumulation of pro-inflammatory senescent cells within tissues is a common hallmark of the aging process and many age-related diseases. This modification has been called the senescence-associated secretory phenotype (SASP) and observed in cultured cells and in cells isolated from aged tissues. Currently, there is a debate whether the accumulation of senescent cells within tissues should be attributed to increased generation of senescent cells or to a defect in their elimination from aging tissues. Emerging studies have revealed that senescent cells display an increased expression of several inhibitory immune checkpoint ligands, especially those of the programmed cell death protein-1 (PD-1) ligand-1 (PD-L1) proteins. It is known that the PD-L1 ligands, especially those of cancer cells, target the PD-1 receptor of cytotoxic CD8+ T and natural killer (NK) cells disturbing their functions, e.g., evoking a decline in their cytotoxic activity and promoting their exhaustion and even apoptosis. An increase in the level of the PD-L1 protein in senescent cells was able to suppress their immune surveillance and inhibit their elimination by cytotoxic CD8+ T and NK cells. Senescent cells are known to express ligands for several inhibitory immune checkpoint receptors, i.e., PD-1, LILRB4, NKG2A, TIM-3, and SIRPα receptors. Here, I will briefly describe those pathways and examine whether these inhibitory checkpoints could be involved in the immune evasion of senescent cells with aging and age-related diseases. It seems plausible that an enhanced inhibitory checkpoint signaling can prevent the elimination of senescent cells from tissues and thus promote the aging process.© 2024. The Author(s).