源于支气管上皮的肺癌是最常见的肺恶性肿瘤。有报道称，程序性细胞死亡1配体1（PD-L1）和肿瘤相关巨噬细胞与肺癌的发展密切相关。然而，肿瘤源性外泌体PD-L1是否能介导肺癌中巨噬细胞极化的调控仍不清楚。本研究使用RT-qPCR评估了正常组织和肺癌组织中的PD-L1水平。然后，使用流式细胞术评估了肺癌细胞的凋亡。随后，使用透射电子显微镜和纳米颗粒跟踪分析观察了囊泡的结构和形态。随后，使用荧光显微镜观察了外泌体被巨噬细胞摄取的情况。我们的结果显示， PD-L1水平在肿瘤组织和肺癌细胞中上调。PD-L1的沉默显著抑制了肺癌细胞的存活能力、迁移和侵袭。此外，肺癌细胞源性外泌体PD-L1能够被巨噬细胞吸收。与此同时，外泌体PD-L1能够促进巨噬细胞M2极化。此外，外泌体PD-L1诱导的巨噬细胞M2极化进一步显著促进了肺癌细胞的存活能力、迁移、侵袭和上皮间质转化过程。总之，PD-L1的沉默显著抑制了肺癌细胞的存活能力、迁移和侵袭。肿瘤细胞源性外泌体PD-L1可以通过介导巨噬细胞M2极化促进肺癌细胞的生长。因此，抑制巨噬细胞M2极化可能是肺癌治疗的一种促进疗法。

Lung cancer originating from the bronchial epithelium is the most common lung malignancy. It has been reported that programmed cell death 1 ligand 1 (PD-L1) and tumor-associated macrophages are closely related to the development of lung cancer. However, whether tumor-derived exosomal PD-L1 could mediate the regulation of macrophage polarization in lung cancer remains unclear. For this research, the level of PD-L1 in normal tissues and lung cancer tissues was evaluated using RT-qPCR. Next, the apoptosis of lung cancer cells was evaluated using flow cytometry assay. Then, the structure and morphology of vesicles were observed using transmission electron microscopy and nanoparticle tracking analysis. Later on, the internalization of exosomes by macrophage was observed using fluorescence microscopy. Our results showed that the level of PD-L1 was upregulated in tumor tissues and lung cancer cells. Knockdown of PD-L1 notably inhibited the viability, migration and invasion of lung cancer cells. In addition, lung cancer cells-derived exosomal PD-L1 could be absorbed by macrophages. Meanwhile, exosomal PD-L1 was able to promote macrophages M2 polarization. Moreover, macrophages M2 polarization induced by exosomal PD-L1 further remarkably promoted the viability, migration, invasion, and epithelial-mesenchymal transition process of lung cancer cells. Collectively, knockdown of PD-L1 notably inhibited the viability, migration and invasion of lung cancer cells. Tumor cell-derived exosomal PD-L1 could promote the growth of lung cancer cells by mediating macrophages M2 polarization. Thus, inhibiting macrophages M2 polarization might be a promoting therapy for the treatment of lung cancer.