期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 38, 期 -, 页码 291-297出版社
ELSEVIER
DOI: 10.1016/j.intimp.2016.06.015
关键词
Natural killer cell; HBsAg; HBeAg; STAT1; NF-kappa B; p38 MAPK
资金
- National Basic Research Program of China [2013CB531503]
- Natural Science Foundation of China [81172789, 30972692]
An 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 NM 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-kappa B and p38 MAPK pathways. These findings implicated that HBV antigen-mediated inhibition of NM 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. (C) 2016 Elsevier B.V. All rights reserved.
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