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Changes of Costimulatory Molecule CD28 on Circulating CD8+T Cells Correlate with Disease Pathogenesis of Chronic Hepatitis B
Author(s) -
Xuefen Li,
Haishen Kong,
Tian Li,
Qiaoyun Zhu,
Yiyin Wang,
Yuejiao Dong,
Qin Ni,
Yu Chen
Publication year - 2014
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2014/423181
Subject(s) - cd28 , cd8 , immunology , cytotoxic t cell , pathogenesis , medicine , antigen , biology , biochemistry , in vitro
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.

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