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Tumor cells primarily employ the PD-1/PD-L1 pathway to thwart the anti-tumor capabilities of T lymphocytes, inducing immunosuppression. This occurs through the direct interaction of PD-L1 with PD-1 on T lymphocyte surfaces. Recent research focusing on the tumor microenvironment has illuminated the pivotal role of immune cells, particularly tumor-associated macrophages (TAMs), in facilitating PD-L1-mediated immunosuppression. Exosomes, characterized by their ability to convey information and be engulfed by cells, significantly contribute to promoting TAM involvement in establishing PD-L1-mediated immunosuppression within the tumor microenvironment. Exosomes, characterized by their ability to convey information and be engulfed by cells, significantly contribute to promoting TAM involvement in establishing PD-L1-mediated immunosuppression within the tumor microenvironment. In addition to receiving signals from tumor-derived exosomes that promote PD-L1 expression, TAMs also exert control over PD-L1 expression in tumor cells through the release of exosomes. This paper aims to summarize the mechanisms by which exosomes participate in this process, identify crucial factors that influence these mechanisms, and explore innovative strategies for inhibiting or reversing the tumor-promoting effects of TAMs by targeting exosomes. [ABSTRACT FROM AUTHOR]

Lung cancer is the leading cause of cancer-related mortality worldwide. The advent of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) has significantly improved survival rates of patients with EGFR-mutant non-small cell lung cancer (NSCLC). However, as with other antitumor drugs, resistance to EGFR-TKIs is inevitably develops over time. Exosomes, extracellular vesicles with a 30–150 nm diameter, have emerged as vital mediators of intercellular communication. Recent studies revealed that exosomes carry non-coding RNAs (ncRNAs), including circular RNA (circRNA), microRNA (miRNA), and long noncoding RNA (lncRNA), which contribute to the development of EGFR-TKIs resistance. This review provides a comprehensive overview of the current research on exosomal ncRNAs mediating EGFR-TKIs resistance in EGFR-mutated NSCLC. In the future, detecting exosome ncRNAs can be used to monitor targeted therapy for NSCLC. Meanwhile, developing therapeutic regimens targeting these resistance mechanisms may provide additional clinical benefits to patients with EGFR-mutated NSCLC. [ABSTRACT FROM AUTHOR]