title: B7-H1 expression is upregulated in peripheral blood CD14+ monocytes of patients with chronic hepatitis B virus infection, which correlates with higher serum IL-10 levels.
abstract: Chronicity in hepatitis B virus (HBV) infection is maintained by increased type 2 T-helper cell response, possibly because of increased interleukin-10 (IL-10) productions. B7-H1 can negatively regulate T-cell responses via its receptor, programmed death 1. Ligation of B7-H1 to T-cells can result in the preferential secretion of IL-10. In this study, we investigated whether there was an upregulated expression of B7-H1 in peripheral blood mononuclear cells in patients chronically infected by HBV and further explored the correlation between B7-H1 expression and serum interleukin 2, interferon-gamma, IL-10, HBeAg, alanine aminotransferase (ALT) levels and viral load. Fifty-five patients with chronic HBV infection and 20 healthy controls (HCs) were enrolled in the present study. The results showed that in patients with chronic hepatitis B CD14+ monocytes but not CD3+ and CD19+ cells had a significantly increased expression of B7-H1 compared with HCs, which positively correlates with serum IL-10 levels and the presence of HBeAg and negatively correlates with serum ALT levels. In conclusion, chronic HBV patients harbour an increased B7-H1 expression in CD14+ monocytes compared with controls, which may be responsible for the increased serum IL-10 levels. This might be an important way by which HBV evades an adequate immune response, leading to viral persistence and disease chronicity.
authors.affiliation: Key Lab of Combined Multi-Organ Transplantation, Ministry of Public Health, First Affiliated Hospital, Zhejiang University School of medicine, Hangzhou 310003, China. geng97927@sohu.com
authors.forename: L
authors.initials: L
authors.lastname: Geng
authors.forename: G
authors.initials: G
authors.lastname: Jiang
authors.forename: Y
authors.initials: Y
authors.lastname: Fang
authors.forename: S
authors.initials: S
authors.lastname: Dong
authors.forename: H
authors.initials: H
authors.lastname: Xie
authors.forename: Y
authors.initials: Y
authors.lastname: Chen
authors.forename: M
authors.initials: M
authors.lastname: Shen
authors.forename: S
authors.initials: S
authors.lastname: Zheng
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000096:biosynthesis / Q000097:blood / Q000276:immunology; D015703:Antigens, CD / Q000096:biosynthesis* / Q000097:blood / Q000276:immunology; D051017:Apoptosis Regulatory Proteins / Q000276:immunology; D060890:B7-H1 Antigen; D005260:Female; D005434:Flow Cytometry; D006513:Hepatitis B e Antigens / Q000096:biosynthesis / Q000097:blood / Q000276:immunology; D006515:Hepatitis B virus / Q000276:immunology / Q000302:isolation & purification*; D019694:Hepatitis B, Chronic / Q000097:blood / Q000276:immunology*; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000097:blood* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D061026:Programmed Cell Death 1 Receptor; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D018418:Th2 Cells / Q000276:immunology; D015854:Up-Regulation
chemical_list: D015703:Antigens, CD; D051017:Apoptosis Regulatory Proteins; D060890:B7-H1 Antigen; C423236:CD274 protein, human; D006513:Hepatitis B e Antigens; D018950:Lipopolysaccharide Receptors; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor; D012333:RNA, Messenger; D016753:Interleukin-10; D000410:Alanine Transaminase