期刊
BMC IMMUNOLOGY
卷 20, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12865-019-0309-9
关键词
CD4(+) T cells; Chronic HBV infection; Inhibitory molecules; Programmed death 1 (PD-1); Lymphocyte activation gene-3 (LAG-3); Cytokine
类别
资金
- Scientific Technology Projects of Health and Family Planning Commission of Zhejiang Province [2017KY066]
- National Natural Science Foundation of China [81672092]
- Major National S&T Projects for Infectious Diseases [2017ZX10202201-002-004]
- Natural Science Foundation of Zhejiang Province [LY15H030012]
Background Immune inhibitory receptors play an important role in chronic infections. However, little is known about their role in hepatitis B virus (HBV) infection. Here, we analyzed the relationship between programmed death-1 (PD-1) and lymphocyte activation gene-3 (LAG-3) expression on CD4(+) T cells and HBV disease progression. Results PD-1 and LAG-3 expression was significantly higher on CD4(+) T cells from HBV patients than on those from the HCs. In addition, a significant positive correlation was found between the PD-1 and LAG-3 expression levels and the ALT(alanine aminotransferase) level. CD4(+) T cell function was inhibited by high PD-1 and LAG-3 levels, and CD4(+) T cells with high PD-1 and LAG-3 expression lost the ability to secrete IFN-gamma, IL-2 and TNF-alpha. Furthermore, blockade of the PD-1 and LAG-3 pathways reversed the damage to CD4(+) T cell proliferation and cytokine secretion. Conclusions CD4(+) T cell exhaustion during chronic HBV had high PD-1 and LAG-3 expression and the absence of helper T cell cytokines, including IFN-gamma, IL-2 and TNF-alpha. After blocking PD-L1 and LAG-3, CD4(+) T cell function in chronic hepatitis B patients was partially restored.
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