Table 2.
Feature of the TME of NSCLC brain metastasis comparing with primary tumor.
| Microenvironment features | Significance | |
|---|---|---|
| T cells | Fewer T cells in total (including Th1 cells or TILs) | Form an immunosuppressed TME, providing a better chance for the tumor growth |
| Lower abundance measurements of Th1 or CD8 T genes | ||
| Inhibition of Th1 immune response | ||
| Macrophage | Higher Gene expression levels of the macrophage (M2-like) marker arginase-I (ARG1) | Present an immunosuppressed TME |
| more anti-inflammatory TAMs | ||
| Lower relative abundances of macrophage genes | ||
| DC | Inhibition of DC maturation | Suppress antigen presentation |
| Lower relative abundances of DC genes | ||
| VCAM1 | Reduced expression of VCAM1 | Suppress adhesion of leukocytes |
| Astrocytes | pSTAT3+ reactive astrocytes | Inhibit CD8+ T cell activation and increase expression of immuno-inhibitory protein PD-L1, promote brain metastasis |
| EVs or gap junctions with tumor cell | Promote the survival of metastasis and increase the resistance of chemotherapy | |
TME, tumor microenvironment; NSCLC, non-small cell lung cancer; type 1 T helper; TILs, tumor Infiltrating Lymphocytes; TAMs, tumor associated macrophages; DC, dendritic cell; VCAM1, vascular cell adhesion molecule 1; pSTAT3, Phosphorylated transducer and activator of transcription-3; PD-L1, programmed death ligand 1; EVs, extracellular vesicles.