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. 2022 Jun 10;23(12):6489. doi: 10.3390/ijms23126489

Figure 1.

Figure 1

Lung microenvironment changes from physiological state to NSCLC development and progression. Normal lung microenvironment includes epithelial cells, smooth muscle cells, fibroblast, endothelial cells, and immune cells such as dendritic cells, neutrophils, T cells, and alveolar macrophages. The latter contribute to maintain immunological homeostasis, but they can also promote inflammation, and thus, development of premalignant lung lesions and carcinogenesis. During NSCLC development, the tumor microenvironment (TME) changes, thus contributing to inflammation angiogenesis, immune modulation, and therefore promoting NSCLC progression, metastasis, and prognosis. In particular, the immune TME, through specific reprogramming and modulation of T cells, tumor-associated macrophages (TAMs) and myeloid cell populations exert crucial tumor-promoting or tumor-suppressing activities. The switch from tumor immune surveillance to cancer immune escape is characterized by the recruitment of regulatory T-cells (Tregs) and upregulation of MDSCs. In addition, TAMs (M1 and M2 polarized cells), and neutrophils play a key role in the mechanisms of immune escape. In particular, they contribute to create a proinflammatory TME that strongly affects the immune response efficiency. Abbreviations: MDSCs—myeloid-derived suppressor cells; IL—Interleukin; VEGF—vascular endothelial growth factor; PD-L—programmed death-ligand; TGF—tumor growth factor; CSF—colony-stimulating factor; M-CSF—macrophage-colony stimulating growth factor. Created with BioRender.com (https://biorender.com/, accessed on 17 May 2022).