Changes of Costimulatory Molecule CD28 on Circulating CD8+ T Cells Correlate with Disease Pathogenesis of Chronic Hepatitis B. (9th June 2014)

• Record Type: Journal Article
• Authors: Li, Xuefen; Kong, Haishen; Tian, Li; Zhu, Qiaoyun; Wang, Yiyin; Dong, Yuejiao; Ni, Qin; Chen, Yu
• Other Names: Schroeder Harry W. Academic Editor.
• Is Part Of: BioMed research international. Volume 2014(2014)
• Publication Date: 2014-06-09
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2014/423181
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Costimulatory signals are critical for antiviral immunity. The aim of this study was to evaluate the change of costimulatory molecule CD28 on circulating CD8 + T cells in chronic hepatitis B patients (CHB). Seventy CHB patients and fifty-six healthy controls were included, and forty-eight CHB patients were recruited for 52 weeks of longitudinal investigation. The proportions of circulating CD8 + CD28 + and CD8 + CD28 − subpopulations were determined by flow cytometry, and the CD8 + CD28 + /CD8 + CD28 − T cells ratio was calculated. Compared with the subpopulation in healthy controls, high proportions of CD8 + CD28 − subpopulation were observed in CHB patients. Similarly, the CD8 + CD28 + /CD8 + CD28 − T cells ratio was significantly decreased in CHB patients compared with healthy controls and correlated significantly with hepatitis B virus (HBV) loads. High proportions of CD8 + CD28 − subpopulation and low CD8 + CD28 + /CD8 + CD28 − T cells ratio were observed in hepatitis B e antigen- (HBeAg-) positive individuals as compared with that in HBeAg-negative subjects. A significant decrease in CD8 + CD28 − subpopulation, increase in CD8 + CD28 + subpopulation, and CD8 + CD28 + /CD8 + CD28 − T cells ratio were seen in those patients who received efficient antiviral therapy. Thus, aberrant CD28 expression on circulating CD8 + T cells and the CD8 + CD28 + /CD8 + CD28 − T cells ratio reflect the dysregulation of T cell activation and are related to the pathogenesis of chronic HBV infection.