Abstract
Tumor-associated macrophages (TAMs), characterized by high plasticity, are the most abundant immune cells in the tumor microenvironment (TME). TAMs are recruited to tumor region in response to various TME components such as cytokines, chemokines as well as exosomes. Subsequently, these environmental cues induce a certain polarization state of TAMs, ranging from anti-tumor states (M1-like) to pro-tumor states (M2-like). Furthermore, the polarization process of TAMs is continuous and gradually inclines toward the M2-like state with malignant progression, forming a positive feedback loop that facilitates tumor growth and metastasis. Consequently, figuring out the factors and mechanisms affecting TAMs polarization is beneficial for developing novel therapeutic strategies that can be combined with other immunotherapies for lung cancer. In previous studies, many significant molecules and pathways which could promote the M2 polarization of TAMs were identified. However, the underlying mechanisms of this sophisticated cross-talk between tumor cells, stroma cells and TAMs remain still difficult to by fully understand. In this review, we summarize the comprehensive factors involved in triggering TAMs polarization towards the M2 phenotype and further explore the relevant molecular mechanisms.
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