Programmed cell death ligand 1 (PD-L1) attenuates the T lymphocytes’ response to tumor cells in various malignancies. Extracellular vesicles (EVs) secreted by effector T cells possess potential as anticancer therapeutics by interaction with tumor cells. Here, we constructed T cell derived EVs which display PD-1, the receptor of PD-L1, on the surface to enhance tumor elimination by interrupting PD-1/PD-L1 pathway. Proteomics analysis indicates that the expression of proteins involved in cytotoxicity, T cell receptor signaling pathway and cell binding were upregulated in PD-1 overexpressing exosomes compared to that of microvesicls. PD-1 expressing EVs (PD-1 EVs) neutralize PD-L1 and effectively reinvigorate the activity and proliferation capacity of CD8⁺ effector T cells. Moreover, PD-1 EVs may also directly attack tumor cells by Fas ligand (FasL) and granzyme B (GzmB).

程序性细胞死亡配体 1 (PD-L1) 减弱了 T 淋巴细胞对各种恶性肿瘤中肿瘤细胞的反应。由效应 T 细胞分泌的细胞外囊泡 (EV) 通过与肿瘤细胞的相互作用具有作为抗癌治疗剂的潜力。在这里，我们构建了 T 细胞衍生的 EV，其在表面显示 PD-1，即 PD-L1 的受体，以通过中断 PD-1/PD-L1 通路来增强肿瘤消除。蛋白质组学分析表明，与微泡相比，过表达 PD-1 的外泌体中与细胞毒性、T 细胞受体信号通路和细胞结合有关的蛋白质的表达上调。表达 PD-1 的 EVs (PD-1 EVs) 中和 PD-L1 并有效重振 CD8 ^{+的活性和增殖能力}效应 T 细胞。此外，PD-1 EVs 还可以通过 Fas 配体 (FasL) 和颗粒酶 B (GzmB) 直接攻击肿瘤细胞。