| 초록 |
Tumor microenvironment (TME) consists of anti-inflammatory factors and immunosuppressive immune cells, such as tumor-associated macrophages (TAMs) and exhausted T cells. Immune checkpoint inhibitors (IC), such as anti PD–L1 antibody (aPD–L1) can revitalize the T cells. However, a current limitation of IC is the TME that attenuates the function of effector T cells. Protumoral M2 TAMs release anti-inflammatory cytokines and impede checkpoint inhibition. In this study, we evaluated the potential therapeutic effects of exosome-mimetic nanovesicles derived from M1 macrophages (M1NVs) to repolarize M2 TAMs to anti-tumoral M1 macrophages. We found that M1NV treatment induced successful repolarization of M2 TAMs to M1 macrophages, and subsequently potentiate the efficacy of aPD-L1 when coinjected. To summarize, we demonstrated that M1NVs can modulate protumoral M2 TAMs to antitumoral M1 macrophages thus acting as an immune adjuvant to overcome the limitation of immune checkpoint inhibitors. |
