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. 2022 Mar 2;28(4):706–724. doi: 10.3350/cmh.2021.0390

Table 2.

EV-mediated communication in regression of chronic liver diseases

EV source Recipient cell Major cargo Effect Reference
NASH
Neutrophil Hepatocyte APOE (surface), miR-223 Decrease expression of inflammatory, lipogenic and fibrogenic genes [118]
Viral hepatitis
Macrophage, LSEC, KC Hepatocyte Anti-HBV molecules (e.g., APOBEC3G, miR-638) Transmit IFN-α-mediated antiviral activity [120]
CD4+ T cell, CD8+ T cell aHSC CD11a (surface) Antifibrogenic responses [122]
Liver fibrosis
qHSC, hepatocyte aHSC Twist1 Antifibrogenic responses [121]
HCC
HCC cell DC AFP, glypican 3 (surface), HSP70 (surface) T cell responses [123]
AFP-expressing DC T cell T cell responses [124]
Drug-treated HCC cell NK cell HSP60, HSP70, HSP90 (surface) NK cell cytotoxicity [125]

EV, extracellular vesicle; NASH, nonalcoholic steatohepatitis; APOE, apolipoprotein E; LSEC, liver sinusoidal endothelial cell; KC, Kupffer cell; HBV, hepatitis B virus; APOBEC3G, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G; IFN, interferon; aHSC, activated hepatic stellate cell; qHSC, quiescent hepatic stellate cell; HCC, hepatocellular carcinoma; DC, dendritic cell; AFP, α-fetoprotein; HSP, heat shock protein; NK, natural killer.