Tumor-associated macrophages (TAMs) are a major component of the tumor microenvironment (TME) and are key cells in regulating tumor development, metastasis, immune responses, inflammation, and chemoresistance. In response to TME stimulation, circulating monocytes are recruited and differentiated as TAMs. Most TAMs are defined as alternatively activated (M2) phenotype to create immunosuppressive TME and support tumor progression. In contrast, classically activated (M1) TAMs can produce pro-inflammatory cytokines and enhance immune responses against tumor development. Autophagy is a conserved catabolic process to control cellular homeostasis and biological function. Emerging evidence reveals crucial contribution of autophagy in modulating TAM plasticity and functional polarization in TME. In this review, we introduce the current understanding of autophagy-regulated TAM function in development of cancer. We focus on how autophagy modulates antigen presentation, LC3-associated phagocytosis, cytokine secretion, inflammasome regulation, recruitment, differentiation, and polarization of TAMs and suggest strategies for potential therapeutics by targeting autophagy in TAMs. We expect this review can provide a new notion of future cancer immunotherapy.

中文翻译：

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自噬驱动肿瘤相关巨噬细胞的可塑性和功能极化

肿瘤相关巨噬细胞 (TAM) 是肿瘤微环境 (TME) 的主要组成部分，是调节肿瘤发展、转移、免疫反应、炎症和化疗耐药的关键细胞。响应 TME 刺激，循环单核细胞被募集并分化为 TAM。大多数 TAM 被定义为交替激活 (M2) 表型，以产生免疫抑制性 TME 并支持肿瘤进展。相比之下，经典激活 (M1) TAM 可以产生促炎细胞因子并增强针对肿瘤发展的免疫反应。自噬是控制细胞稳态和生物学功能的保守分解代谢过程。新出现的证据揭示了自噬在调节 TME 中 TAM 可塑性和功能极化方面的重要贡献。在本次审查中，我们介绍了目前对自噬调节的 TAM 功能在癌症发展中的理解。我们专注于自噬如何调节抗原呈递、LC3 相关吞噬作用、细胞因子分泌、炎症小体调节、募集、分化和 TAM 的极化，并通过靶向 TAM 中的自噬提出潜在治疗策略。我们希望这篇综述可以为未来的癌症免疫治疗提供一个新的概念。