Intrahepatic levels of PD-1/PD-L correlate with liver inflammation in chronic hepatitis B

Abstract

These results suggest that over-expression of PD-1, PD-L1 and PD-L2 within liver may participate in local immune dysfunction, which could be one of the mechanisms involved in the chronicity of HBV infection and chronic inflammation seen in CHB patients.

The Role of LAT in Increased CD8 + T Cell Exhaustion in Trigeminal Ganglia of Mice Latently Infected with Herpes Simplex Virus 1

“…It was therefore of interest to determine the functional significance of high PD-1 expression (PD-1 high ) during HSV latency. CD8 T cell exhaustion plays a major role in chronic infection with LCMV, and both PD-1 and its ligands are major markers of exhaustion and play a functional role in this exhaustion (5,9,79). In vivo administration of anti-PD-1 or anti-PD-L1 antibody that blocked the interaction of PD-1 with its ligand, PD-L1, enhanced T cell responses and clearance of LCMV (5), hepatitis C virus (HCV) (73), and HIV (66).…”

Kupffer cell in the immune activation and tolerance toward HBV/HCV infection

“…The level of PD-1, PD-L1 and PD-L2 in patients suffering chronic hepatitis is much higher than that in healthy people, and correlates with the severity of the disease. 42 In infections or inflammations, KCs inhibit the replication of activated T cells and their immune function through the PD-1/PD-L1 signaling pathway and interaction between cells mediated by the T cell immunoglobulin and mucindomain containing-3 (TIM-3) protein. An increase in ga-pase-1 or the NLRP3 inflammasome in KCs, eventually causing inflammation and fibrogenesis.…”

Mechanism of Kupffer cells in hepatitis infected by hepatitis B and C virus

“…The level of PD-L1,PD-L2 and PD-1 are all higher in the chronic HBV / HCV infected patients in comparison with healthy individuals, and are considered to have relations to the severity of the infection. [28] And the continuous presentation of inhibitors such as PD-1 and TIM-3 might involve with the function and exhaustion of CD+8 T and CD+4 T. 29 Nevertheless, the up-regulation of inhibitory receptors,which are based on the macrophages of the liver and the inflammatory activities involved with macrophages caused directly by the infection of HBV/HCV or by the mechanism of negative feedback after ongoing inflammation, still remains uncertain.…”