Functional effects of killer cell lectin-like receptor subfamily G member 1 on natural killer cells in chronic hepatitis B infection
10.3760/cma.j.issn.1007-3418.2018.08.005
- VernacularTitle: 杀伤细胞凝集素样受体亚家族G成员1在慢性乙型肝炎病毒感染中对自然杀伤细胞功能的影响
- Author:
Minghong LI
1
;
Qiongfang ZHANG
;
Wenwei YIN
;
Dazhi ZHANG
;
Hong REN
Author Information
1. Department of Infectious Diseases, Institute of Viral Hepatitis, Key Laboratory of Molecular Biology of Infectious Diseases, Chinese Ministry of Education, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
- Publication Type:Journal Article
- Keywords:
Hepatitis B virus;
Interferon-gamma;
Nature killer cell;
Killer cell lectin-like receptor subfamily G member 1
- From:
Chinese Journal of Hepatology
2018;26(8):585-589
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the functional effects of killer cell lectin-like receptor subfamily G member 1 (KLRG1) expression on natural killer cells (NK cell) in chronic hepatitis B virus infection (HBV).
Methods:Peripheral blood mononuclear cells (PBMC) were extracted from 120 patients with chronic hepatitis B virus infection and 19 healthy persons. The frequency of NK cells and KLRG1+ NK cells in peripheral blood was detected by flow cytometry. Interferon-γ levels secreted by NK cells were detected in peripheral blood. Statistical analysis of experimental data was performed using GraphPad Prism 6.03 software.
Results:The frequency of NK cells in HBV-infected group (16.92% ± 7.9%) was not significantly different from that in healthy controls (10.57% ± 6.5%). The frequency of KLRG1+NK cells in HBV-infected group was significantly higher (49.43% ± 21.2%) than that to healthy control group (31.60% ± 17.9%), (t = 7.347 6, P < 0.001). IFN-γ secretion of KLRG1 + NK cells in HBV-infected patients (2.59% ± 1.0%) were significantly lower than healthy controls (5.96% ± 2.4%), (P = 0.009).
Conclusion:HBV infection can increase the expression of KLRG1 in NK cells and further reduce the secretion of IFN-γ in NK cells, which may be an important cause for chronic HBV infection.
