a | Scavenger sinusoidal cell populations, such as Kupffer cells, phagocytose circulating bacteria and crosstalk with natural killer T (NKT) cells to generate strong intravascular pathogen-specific immune responses. Inhibiting the access of pathogens to hepatocytes may have an important role in preventing the development of persistent hepatic infections. b | The death of infected hepatocytes during viral replication may cause the activation of Kupffer cells or dendritic cells (DCs), which in turn promote the killing of other hepatocytes through CD95 (also known as FAS) and the release of pro-inflammatory mediators. Material from dying virus-infected cells increases cross-priming by DCs and thereby augments pathogen-specific adaptive immunity98, 175. Combinatorial stimulation by pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), such as ATP, may allow immune-mediated control of established hepatic infections. CXCL9, CXC-chemokine ligand 9; CXCR3, CXC-chemokine receptor 3; IFN, interferon; IL, interleukin; LSEC, liver sinusoidal endothelial cell; TCR, T cell receptor; TNF, tumour necrosis factor.