Autophagy is catabolic process by degradation of intracellular components in lysosome including proteins, lipids, and mitochondria in response to nutrient deficiency or stress such as hypoxia or chemotherapy. Increasing evidence suggests that autophagy could induce immune checkpoint proteins (PD-L1, MHC-I/II) degradation of cancer cells, which play an important role in regulating cancer cell immune escape. In addition to autophagic degradation of immune checkpoint proteins, autophagy induction in immune cells (macrophages, dendritic cells) manipulates antigen presentation and T cell activity. These reports suggest that autophagy could negatively or positively regulate cancer cell immune escape by immune checkpoint protein and antigens degradation, cytokines release, antigens generation. These controversial phenomenon of autophagy on cancer cell immune evasion may be derived from different experimental context or models. In addition, autophagy maybe exhibit a role in regulating host excessive immune response. So rational combination with autophagy could enhance the efficacy of cancer immunotherapy. In this review, the current progress of autophagy on cancer immune escape is discussed.

中文翻译：

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自噬在癌症免疫逃逸中的作用

自噬是通过降解溶酶体中的细胞内成分（包括蛋白质、脂质和线粒体）来响应营养缺乏或应激（例如缺氧或化疗）的分解代谢过程。越来越多的证据表明，自噬可以诱导癌细胞的免疫检查点蛋白（PD-L1、MHC-I/II）降解，这在调节癌细胞免疫逃逸中起重要作用。除了免疫检查点蛋白的自噬降解外，免疫细胞（巨噬细胞、树突状细胞）中的自噬诱导还可以控制抗原呈递和 T 细胞活性。这些报告表明，自噬可以通过免疫检查点蛋白和抗原降解、细胞因子释放、抗原产生来负向或正向调节癌细胞的免疫逃逸。这些有争议的自噬对癌细胞免疫逃避的现象可能源于不同的实验背景或模型。此外，自噬可能在调节宿主过度免疫反应中发挥作用。因此合理结合自噬可以增强肿瘤免疫治疗的疗效。本综述就自噬在癌症免疫逃逸中的研究进展进行了讨论。