共抑制通路和细胞免疫失衡HBV感染的进展

StephenW

Hepatology International
January 2014, Volume 8, Issue 1, pp 55-63
The co-inhibitory pathway and cellular immune imbalance in the progress of HBV infection

    Jie Chen,
    Lanlan Wang,
    Yang Fu,
    Yi Li,
    Yangjuan Bai,
    Limei Luo,
    Yun Liao


Abstract
Objective

Chronic hepatitis B (CHB) affects 400 million people and is the most common cause of liver cirrhosis (LC) and hepatocellular carcinoma (HCC) worldwide. Cellular immune regulation plays an important role in determining the infection outcome. Co-signal molecules and Th17/Treg were studied to explore their association with the progression of HBV infection.
Methods

Ninety-four HBV-infected patients were categorized into three groups: 31 patients with LC caused by CHB, 30 with HCC caused by CHB and 33 with HCC caused by CHB. Co-signal molecules, Th17/Treg, and Stat3 and Stat5 were analyzed by flow cytometry.
Results

CHB patients who progressed to LC or HCC showed a significantly higher level of co-inhibitory molecules such as BTLA and PD-1, while there was no significant difference in co-stimulatory molecules among LC, HCC and CHB. Stat3 and Stat5 were significantly increased in LC and HCC compared to CHB patients.
Conclusion

Co-inhibitory molecules play more important roles than co-stimulatory molecules. Increased PD-1 and BTLA/HVEM inhibited immune cells and the immune process. At the same time activated Stat3 and Stat5 stimulate the key factors in differentiation of Th17 and Treg, thus leading to imbalanced expansion of Th17 and Treg; immune tolerance was induced and HBV persistent. This resulted in hepatic inflammation that progressed to cirrhosis and carcinoma.

StephenW

国际肝病
2014年1月，第8卷，第1期，页55-63
共抑制通路和细胞免疫失衡HBV感染的进展

    陈杰，
    兰兰王，
    杨富，
    易立，
    羊圈白，
    丽美罗，
    恽哩翱


摘要
目标

慢性乙型肝炎（CHB ）影响4亿人，是肝硬化（LC ）的最常见的原因和世界各地的肝细胞癌（HCC ） 。细胞免疫调节起着决定的感染结局的重要作用。共同的信号分子和Th17/Treg的进行了研究，以探讨其协会与HBV感染的进展。
方法

九十四HBV感染患者分为三组： 31例LC引起的慢性乙型肝炎， 30引起的​​慢性乙型肝炎和33与肝癌引起的慢性乙型肝炎肝癌。共同的信号分子， Th17/Treg的，和STAT3和Stat5的流式细胞术分析。
结果

CHB患者谁发展到LC或HCC呈协同抑制分子，如BTLA和PD - 1的显著更高的水平，同时有LC ， HCC和CHB之间的共刺激分子无显著差异。 Stat3与Stat5的进行了比较， CHB患者在肝硬化和肝癌显著增加。
结论

联合抑制分子发挥比共刺激分子更加重要的作用。提高PD- 1和BTLA / HVEM抑制免疫细胞和免疫过程。同时激活的Stat3和Stat5的刺激的关键因素Th17细胞和调节性T细胞的分化，从而导致Th17细胞和调节性T细胞的不平衡扩大;免疫耐受的诱导和HBV持续性。这导致在肝脏炎症进展到肝硬化和肝癌。

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