乙型肝炎病毒抗原削弱NK细胞的功能。

StephenW

Int Immunopharmacol. 2016 Jun 21;38:291-297. doi: 10.1016/j.intimp.2016.06.015. [Epub ahead of print]
Hepatitis B virus antigens impair NK cell function.Yang Y1, Han Q2, Zhang C2, Xiao M3, Zhang J4.
Author information

• 1State Key Lab of Microbial Technology, National Glycoengineering Research Center, Shandong University, China; Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University, China.
• 2Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University, China.
• 3State Key Lab of Microbial Technology, National Glycoengineering Research Center, Shandong University, China; Shandong Provincial Key Laboratory of Carbohydrate Chemistry and Glycobiology, Shandong University, China. Electronic address: [email protected].
• 4Institute of Immunopharmaceutical Sciences, School of Pharmaceutical Sciences, Shandong University, China. Electronic address: [email protected].
  

AbstractAn inadequate immune response of the host is thought to be a critical factor causing chronic hepatitis B virus (CHB) infection. Natural killer (NK) cells, as one of the key players in the eradication and control of viral infections, were functionally impaired in CHB patients, which might contribute to viral persistence. Here, we reported that HBV antigens HBsAg and HBeAg directly inhibited NK cell function. HBsAg and/or HBeAg blocked NK cell activation, cytokine production and cytotoxic granule release in human NK cell-line NK-92 cells, which might be related to the downregulation of activating receptors and upregulation of inhibitory receptor. Furthermore, the underlying mechanisms likely involved the suppression of STAT1, NF-κB and p38 MAPK pathways. These findings implicated that HBV antigen-mediated inhibition of NK cells might be an efficient strategy for HBV evasion, targeting the early antiviral responses mediated by NK cells and resulting in the establishment of chronic virus infection. Therefore, this study revealed the relationship between viral antigens and human immune function, especially a potential important interaction between HBV and innate immune responses.
Copyright © 2016 Elsevier B.V. All rights reserved.


KEYWORDS: HBeAg; HBsAg; NF-κB; Natural killer cell; STAT1; p38 MAPK

StephenW

诠释Immunopharmacol。 2016年6月21日; 38：291-297。 DOI：10.1016 / j.intimp.2016.06.015。 [打印EPUB提前]
乙型肝炎病毒抗原削弱NK细胞的功能。
杨Y1，韩Q2，张C2，肖M3，张J4。
作者信息

    微生物技术国家糖工程技术研究中心，山东大学，中国的国家重点实验室;山东大学免疫药物科学研究所，药学院，中国。
    免疫药物学，药学院，山东大学，中国的2Institute。
    微生物技术国家糖工程技术研究中心，山东大学，中国的3STATE重点实验室;糖化学及糖生物学，山东大学，中国山东省重点实验室。电子地址：[email protected]~~V。
    免疫药物学，药学院，山东大学，中国的4Institute。电子地址：[email protected]。

抽象

主机的不足的免疫应答被认为是引起慢性乙型肝炎病毒（CHB）感染的关键因素。自然杀伤（NK）细胞，在消灭和病毒感染控制的关键球员之一，在功能CHB患者，这可能会助长病毒的持久性损害。在这里，我们报道了HBV抗原HBsAg和HBeAg直接抑制NK细胞的功能。 HBsAg和/或HBeAg的阻断NK细胞活化，细胞因子的产生和细胞毒性颗粒释放在人NK细胞系的NK-92细胞，其可能与激活受体和抑制性受体的上调的下调。此外，潜在的机制可能涉及STAT1，NF-κB和p38 MAPK通路的抑制。这些发现暗示了NK细胞的HBV抗原介导的抑制可能是乙肝病毒逃避一种有效的策略，指定由NK细胞介导的​​，并导致建立慢性病毒感染的早期抗病毒反应。因此，本研究揭示了病毒抗原与人体免疫功能，尤其是乙肝病毒和先天免疫反应之间的潜在的重要的互动关系。

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关键词：

大三阳;乙肝表面抗原; NF-κB;自然杀伤细胞; STAT1; p38蛋白