Roles and application of exosomes in the development, diagnosis and treatment of gastric cancer

Table 1 Exosome-mediated regulation of immunity

Origin of exosomes	Target cells	Functional molecules	Mechanisms	Ref.
DC	CD4 and CD8+ T cells	CD80 and IL-2	Induce anti-tumor immune response	[18]
Treg	T cells and B cells	IL-35	Induce peripheral tolerance of T cells and B cells by transferring IL-35	[21]
Treg	Th-1	Let-7d	Inhibition of Th1 cell proliferation and cytokine release	[22]
TAM	CD4+ T cells	miR-29a-3p miR-21-5p	Induce Treg/Th17 imbalance	[25]
NK	T cells	miR-186	Inhibition of tumorigenic potential and TGFβ-dependent immune escape	[31]
TDE	CD4 and CD8+ T cells	IL-2	Inhibition of IL-2-mediated proliferation of CD4 and CD8 T cells	[34]
TDE	T cells	FasL and CD3-ζ	Induce T cell apoptosis or inhibit T cell receptor signaling	[35]
GC-exosomes	T cells	PI3K proteasome and caspases 3, 8, 9	Mediate degradation of PI3K proteasome and activation of caspases 3, 8 and 9, and induce apoptosis of Jurkat T cells	[36]
GC-exosomes	CD8+ T cells	IL-10	Inducing PD1 signal can effectively enhance the immunosuppressive activity	[37]
GC-exosomes	MSCs	NF-κB signaling pathway	Promote macrophage phagocytosis, up-regulate the secretion of proinflammatory factors and promote the activation of CD69 and CD25	[38]
TDE	DC	miR-212-3p	Inhibit MHC II transcription factor RFXAP in dendritic cells	[39]

DC: Dendritic cell; IL: Interleukin; Treg: Regulatory T cell; Th1: Type 1 T helper; TAM: Tumor-associated macrophage; NK: Natural killer; TGF: Transforming growth factor; TDE: Tumor-derived exosome; GC: Gastric cancer; PD1: Programmed cell death 1; MSC: Mesenchymal stem cell; NF-κB: Nuclear factor kappa-beta; MHC: Major histocompatibility complex; FasL: Fas ligand.