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Gut Liver. 2014 Mar;8(2):186-95. doi: 10.5009/gnl.2014.8.2.186. Epub 2013 Dec 24.

The expression of programmed death-1 in circulating CD4+ and CD8+ T cells during hepatitis B virus infection progression and its correlation with clinical baseline characteristics.

Author information

1
The Affiliated Infectious Hospital of Soochow University, Suzhou, China. ; Key Laboratory of Infection and Immunity of Suzhou City, Suzhou, China.
2
Key Laboratory of Infection and Immunity of Suzhou City, Suzhou, China. ; Medical Biotechnology Institute, Medical College of Soochow University, Suzhou, China.
3
Medical Biotechnology Institute, Medical College of Soochow University, Suzhou, China. ; School of Biology and Basic Medical Sciences, Medical College of Soochow University, Suzhou, China.

Abstract

BACKGROUND/AIMS:

Programmed death-1 (PD-1) expression was investigated in CD4(+) and CD8(+) T cells from hepatitis B virus (HBV)-infected patients at the chronic hepatitis B (CHB) infection, liver cirrhosis (LC), and hepatocellular carcinoma (HCC) stages.

METHODS:

PD-1 expression in circulating CD4(+) and CD8(+) T cells was detected by flow cytometry. The correlations between PD-1 expression and HBV viral load, alanine aminotransaminase (ALT) levels and aspartate aminotransferase (AST) levels were analyzed using GraphPad Prism 5.0.

RESULTS:

PD-1 expression in CD4(+) and CD8(+) T cells was significantly increased in both the CHB group and advanced-stage group (LC plus HCC). In the CHB group, PD-1 expression in both CD4(+) and CD8(+) T cells was positively correlated with the HBV viral load, ALT, and AST levels. However, in the LC plus HCC group, significant correlations between PD-1 expression and the clinical parameters were nearly absent.

CONCLUSIONS:

PD-1 expression in peripheral CD4(+) and CD8(+) T cells is dynamic, changes with HBV infection progression, and is related to HBV viral load and liver function, especially in CHB. PD-1 expression could be utilized as a potential clinical indicator to determine the extent of virus replication and liver injury.

KEYWORDS:

Carcinoma, hepatocellular; Hepatitis B virus; Hepatitis B, chronic; Liver cirrhosis; Programmed death-1

PMID:
24672661
PMCID:
PMC3964270
DOI:
10.5009/gnl.2014.8.2.186
[Indexed for MEDLINE]
Free PMC Article
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