Fig. 3

Tumor-derived exosomes inhibit normal function of dendritic cells. A plethora of inhibitory molecules including PD-L1, CD73, IDO (Indoleamine 2, 3-dioxygenase), L-arginase, PGE2, TGF-β, Lipids, and components of the STAT3 activators is presented in TDEs can reprogram DCs into immunosuppressive players and subvert their function either in priming or sustaining of anti-tumor immune responses. Exosomal PD-L1 interacts with PD-1 expressed on immune cells, including DCs and inhibits their function. IDO and L- arginase degrades tryptophan and arginine, respectively and thereby impedes effective priming of T cells. PGE2 and TGF- β are two inhibitory molecules enriched in TDEs which can impair antigen-presentation activity of DCs. Lipids and the STAT3 activating components can also be transported by TDEs, inducing dysfunctional DCs