Chemokine Receptor Expression of Hepatitis B Virus-Specific CD8+ Lymphocyte in Chronic B Viral Infection.
- Author:
Chun Kyon LEE
1
;
Jeong Hun SUH
;
Young Suk CHO
;
Kwang Hyub HAN
;
Jae Bock CHUNG
;
Chae Yoon CHON
;
Young Myoung MOON
Author Information
1. Department of Internal Medicine, National health insurance corporation Ilsan Hospital1, Koyang, Korea. cklee33@nhimc.or.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Hepatitis/Viral/Chronic hepatitis B;
HBV-specific CD8+ lymphocyte;
Chemokine receptor
- MeSH:
CD8-Positive T-Lymphocytes/immunology/*metabolism;
English Abstract;
Hepatitis B Virus/immunology;
Hepatitis B, Chronic/*immunology/pathology;
Human;
Liver/pathology;
Receptors, CCR5/metabolism;
Receptors, Chemokine/*metabolism;
T-Cell Antigen Receptor Specificity
- From:The Korean Journal of Hepatology
2002;8(4):363-370
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: The protective role of HBV-specific CD8+ cells is dependent on their ability to efficiently migrate to the infected liver, where they may exert an effector function. The migratory behavior of CD8+ cells is influenced by their expression of different chemokine receptors. This study was intended to analyse the pattern of chemokine receptor expression of HBV specific CD 8+ cells in chronic B viral infection. METHODS: We analysed the CCR5 and CCR3 profile of HBV-specific CD8+ cells isolated from the blood and liver of patients with different patterns of HBV infection. Purified T cells were stained directly ex vivo, or after antigen-specific stimulation, using HBV peptide-specific HLA tetramers and monoclonal antibodies to CD8, CCR5 and CCR3, with analysis by flow cytometry. RESULTS: In patients with chronic hepatitis B characterised by low levels of virus (serum HBV DNA <0.5pg/mL) and minimal liver inflammation, analysis of circulating and intrahepatic CD8+ cells demonstrated that liver infiltrating Tc18-27-specific cells were preferentially CCR5+ (up to 80% of HBV-specific CD8+ cells), in contrast to cells of the same specificity within the circulating compartment (up to 35% of HBV-specific CD8+ cells). Furthermore, CCR3 was expressed by about 10% of Tc18-27+ cells infiltrating the liver, but was absent from circulating cells. Following HBV-specific stimulation in vitro the CCR5 expression of circulating Tc18-27-specific cells was up-regulated, to levels found in liver infiltrating cells, whereas CCR3 expression was unchanged. CONCLUSIONS: The chemokine receptor profile of HBV-specific CD8+ cells is influenced by the anatomical site of these cells, and the clinical pattern of disease. The ability of circulating HBV-specific CD8+ cells of patients with low replicating virus to upregulate CCR5 suggests that these cells may respond to increases in virus replication by efficiently migrating into the infected liver.
