Fig. 3

ILCs in hepatic viral infections.A MCMV infection induces the expression of proinflammatory cytokines, including IL-12, type I interferon (IFN-I), and IL-18, which regulate type I ILCs. ILC1s recognize MCMV-encoded m12 on infected cells through NKRP-1 receptors and restrict the viral load in an IFNγ-dependent manner. In response to MCMV infection, ILC1s expand and form adaptive compartments with increased effector functions. NK cells recognize MCMV-encoded m157 through the Ly49H activation receptor. NK cell-mediated viral control in the liver relies more on IFNγ and less on direct lysis than in the spleen. Hepatic NK cells also expand in response to MCMV infection, which is required for long-term viral control in the liver but not in the spleen. B Hepatitis B virus (HBV) infection results in the recruitment of CD56bright NK cells to the liver, where they potentially promote liver damage. In chronic HBV infection, NK cells display a reduced capacity to produce IFNγ but they have the capacity to restrain HBV-specific CD8 + T-cell responses in a TRAIL-dependent manner. C Control of hepatitis C virus (HCV) infection has been genetically associated with the inhibitory receptor KIR2DL3 and its ligand human leukocyte antigen (HLA)-C1. HCV infection induces an activated phenotype and expansion of KIR2DL3 NK cells in the peripheral blood. However, their role within the hepatic microenvironment requires elucidation