Table 1.

Overview of findings on NK–DC crosstalk in liver cancer.

Pathology	Dysfunction	Effect	Reference
Chronic HCV infection	↑ NKG2A expression and ↑ production of IL-10 and TGF-β by NK cells	NK cells were not able to activate DCs	[188,189]
HCV infection	Aberrant expression of MICA/B on DCs due to impaired IL-15 production	↓ NKG2D-mediated NK cell activation	[188,189]
Chronic HBV infection	Defective responses of pDCs upon TLR9 stimulation	Aberrant NK cells activation	[190]
HCC	↑ sMICA is associated with ↓ NKG2D and impaired activation of NK cells	Abolished maturation and activation of DCs	[191,192]
HCC	AFP inhibits IL-12 production by DCs	↓ NK cytotoxic activity against tumor cells	[82,193]
HCC	LAMP3+ DCs expressing NECTIN might interact with DNAM-1 expressed on the blood-circulating NK cells; LAMP3+ DCs expressing NECTIN might interact with TIGIT expressed on lr-NK cells	Activating signal Inhibitory signal	[183]
ICC	↓ TNF-α-producing DCs	Impaired activation of NK cells	[179]

HCV = Hepatitis C virus, HBV = Hepatitis B virus, HCC = Hepatocellular carcinoma, and ICC = Intrahepatic cholangiocarcinoma. The ↑ symbol indicates an increase in frequency or expression levels and the ↓ symbol indicates a decrease in frequency or expression levels.