Figure 3.

Crosstalk between BCSCs and immune cells in the TME. BCSCs can escape immune surveillance by regulating their surface ligands to suppress the immune response. The expression of ULBP and MICA/B is reduced to suppress the binding with NK cell receptors and evade NK cell-mediated cell killing. Antigen-presenting capacity is decreased to prevent the effector T-cell activation. PD-L1 and CD47 are overexpressed in BCSCs to suppress the anti-tumor effects of T cells and macrophages respectively. Additionally, BCSCs can recruit nonlytic CD8 T cells, Treg cells, and neutrophils to enhance self-renewal and metastatic abilities. Last but not least, an immunosuppressive niche is constituted by recruiting and activating the immunosuppressive cell population, including TAM, Treg cells, and neutrophils.