Table 3.

Role of EVs- PD-L1 in immune escape

Cancer type	Function	Mechanism	Ref
Glioblastoma	Promoted monocytes toward the immune suppressive M2 phenotype and caused immune suppressive function	Up-regulated PD-L1 expression and activated STAT3 pathway	[71]
Breast	Induced an immunosuppressive microenvironment that encourages tumor development	PD-L1 inhibited CD8 + T cells function and polarized macrophages into M2-type	[72]
Gastric	Caused T-cell dysfunction	MHC-I stimulated impaired T cells function	[73]
	Prompt expression of PD-L1 on neutrophils to overturn T-Cell activity	HMGB1 promoted the expression of PD-L1 in neutrophils Triggered STAT3 signaling	[74]
Hepatocellular	Suppressed CD8 + T cells and promoted PD-L1 stabilization	Up-regulated PD-L1 on macrophages by GOLM1	[75]
Head and neck	Impaired the activity of effector T cells	Suppressed CD69 expression	[76]
Non-small cell lung	Induced CD8 + T cells death and tumor development	Suppressed production of IL-2 and IFN-γ by CD8 + T cells/ Reduced number of CD8 + T cells	[77]
	Promoted tumor metastasis	Activated NF-κB signaling and glycolysis dominated metabolic reprogramming pathway that induced the PD-L1 expression level in macrophages	[78]
Lung	Improved tumor growth in vivo	Inhibited cytokine production/ Promoted apoptosis in CD8 + T cells	[60]
Chronic lymphocytic leukemia	Promoted cancer cells escape from antitumor immunity	Induced the PD-L1 levels in macrophages/Increased miR-23a-3p in EVs/ Activated PTEN-AKT axis	[79]
	Inhibited tumor immunity	hY4 in EVs from CLL patients interact with TLR7 on monocytes, thus promoting the expression of inflammatory factors and PD-L1 in monocytes	[80]