title: [Chemokine receptor expression of hepatitis B virus-specific CD8+ lymphocyte in chronic B viral infection].
abstract: OBJECTIVE
  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 <0.5 pg/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.
authors.affiliation: Department of Internal Medicine, National health insurance corporation Ilsan Hospital, Koyang, Korea. cklee33@nhimc.or.kr
authors.forename: Chun Kyon
authors.initials: CK
authors.lastname: Lee
authors.forename: Jeong Hun
authors.initials: JH
authors.lastname: Suh
authors.forename: Young Suk
authors.initials: YS
authors.lastname: Cho
authors.forename: Kwang-Hyub
authors.initials: KH
authors.lastname: Han
authors.forename: Jae Bock
authors.initials: JB
authors.lastname: Chung
authors.forename: Chae Yoon
authors.initials: CY
authors.lastname: Chon
authors.forename: Young Myoung
authors.initials: YM
authors.lastname: Moon
mesh_terms: D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D006515:Hepatitis B virus / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000276:immunology* / Q000473:pathology; D006801:Humans; D008099:Liver / Q000473:pathology; D054397:Receptors, CCR3; D019713:Receptors, CCR5 / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism*; D037182:T-Cell Antigen Receptor Specificity
chemical_list: C515350:CCR3 protein, human; D054397:Receptors, CCR3; D019713:Receptors, CCR5; D019707:Receptors, Chemokine