M1 Macrophage-Derived Nanovesicles Potentiate the Anticancer Efficacy of Immune Checkpoint Inhibitors

免疫系统 癌症研究 肿瘤微环境 巨噬细胞极化 巨噬细胞 免疫疗法 免疫检查点 医学 免疫学 体外 生物 生物化学
作者
Yeon Woong Choo,Mikyung Kang,Han Young Kim,Jin Han,Seokyung Kang,Ju‐Ro Lee,Gun‐Jae Jeong,Sung Pil Kwon,Seuk Young Song,Seokhyeong Go,Mungyo Jung,Jihye Hong,Byung‐Soo Kim
出处
期刊:ACS Nano [American Chemical Society]
卷期号:12 (9): 8977-8993 被引量:347
标识
DOI:10.1021/acsnano.8b02446
摘要

Cancer immunotherapy modulates immune cells to induce antitumor immune responses. Tumors employ immune checkpoints to evade immune cell attacks. Immune checkpoint inhibitors such as anti-PD-L1 antibody (aPD-L1), which is being used clinically for cancer treatments, can block immune checkpoints so that the immune system can attack tumors. However, immune checkpoint inhibitor therapy may be hampered by polarization of macrophages within the tumor microenvironment (TME) into M2 tumor-associated macrophages (TAMs), which suppress antitumor immune responses and promote tumor growth by releasing anti-inflammatory cytokines and angiogenic factors. In this study, we used exosome-mimetic nanovesicles derived from M1 macrophages (M1NVs) to repolarize M2 TAMs to M1 macrophages that release pro-inflammatory cytokines and induce antitumor immune responses and investigated whether the macrophage repolarization can potentiate the anticancer efficacy of aPD-L1. M1NV treatment induced successful polarization of M2 macrophages to M1 macrophages in vitro and in vivo. Intravenous injection of M1NVs into tumor-bearing mice suppressed tumor growth. Importantly, injection of a combination of M1NVs and aPD-L1 further reduced the tumor size, compared to the injection of either M1NVs or aPD-L1 alone. Thus, our study indicates that M1NV injection can repolarize M2 TAMs to M1 macrophages and potentiate antitumor efficacy of the checkpoint inhibitor therapy.
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