Costimulatory molecule programmed death-1 in the cytotoxic response during chronic hepatitis C

Figure 2 Liver microenvironment. Circulating HCV-specific CD8⁺ T cells migrating through the hepatic sinusoid interact with resident liver cells [Kupffer cells, dendritic cells (DC), hepatocytes, liver sinusoidal endothelial cells (LSECs), stellate cells] that could act as antigen presenting cells. These cells up-regulate PD-L1 expression during persistent HCV infection and interact with the PD-1 molecule expressed on HCV-specific CD8⁺ T cells. This interaction leads to T cell anergy. PD-1 up-regulation is produced by TCR stimulation in addition to the interaction between HCV-core protein and the complement receptor (gC1qR). In this micro-environment the regulatory T cells (Treg) also participate, whose activity is also regulated by the PD-1/PD-L1 pathway.