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   <subfield code="a">Intrahepatic levels of PD-1/PD-L correlate with liver inflammation in chronic hepatitis B</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Ji Chen, Xiao-Mei Wang, Xue-Jie Wu, Yan Wang, Hong Zhao, Bing Shen, Gui-Qiang Wang]</subfield>
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   <subfield code="a">Background and objective: Programed cell death-1 (PD-1) represents a mechanism of T-cell dysfunction in hepatitis B virus (HBV) persistence. In peripheral blood, PD-1 is up-regulated in virus-specific T cells, leading to the impairment of T cells. This study investigated the intrahepatic expression of PD-1 and its ligand (PD-L) in patients with chronic hepatitis B (CHB) virus. Methods: Liver specimens were obtained from CHB (n=56), acute hepatitis B (AHB, n=12) patients and age-matched healthy subjects (n=10). The expression of PD-1/PD-L was determined by immunohistochemistry. Results: In CHB patients, PD-1 was predominantly expressed in lymphocytes infiltrating the portal tract. PD-L1 was detected in lymphocytes, hepatocytes and liver sinusoidal endothelial cells, while PD-L2 was localized in Kupffer cells and dendritic cells. The labeling indexes of PD-1 and PD-L1 in lymphocytes infiltrating portal area were significantly higher in CHB patients than in healthy controls and AHB patients. Within the CHB patients, the increases in labeling indexes of PD-1 and PD-L paralleled the degree of inflammation. Conclusions: 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.</subfield>
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   <subfield code="a">Chronic hepatitis B</subfield>
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