Figure 6.

Regulation of ILC activity by tumor-derived EVs. Exposure of NK cells to tumor-derived EVs may lead to increased anti-tumor activity but also decreased immunoreactivity. The presence of Hsp70 (A) or ligands that activate the NK receptor (NKl) (B) have been proposed as mechanisms driving NK-cell activation, proliferation, and tumor-cell death. Nevertheless, the presence of NKls on tumor-secreted EVs may also lead to the opposite effect (C) if behaving as a decoy for the activation of NK receptors (NKr). EVs carrying TFGβ (T) (D) decrease NKr content on NK cells, which blocks NK-cell activation as well as the recognition of NKl-presenting tumor cells.