Chronic hepatitis C viral infection reduces NK cell frequency and suppresses cytokine secretion: Reversion by anti-viral treatment

被引:57
作者
Dessouki, Omar [1 ]
Kamiya, Yasuyuki [2 ]
Nagahama, Hiroyasu [2 ]
Tanaka, Motohiko [2 ]
Suzu, Shinya [1 ]
Sasaki, Yutaka [2 ]
Okada, Seiji [1 ]
机构
[1] Kumamoto Univ, Div Hematopoiesis, Ctr AIDS Res, Kumamoto 8600811, Japan
[2] Kumamoto Univ, Dept Gastroenterol & Hepatol, Grad Sch Med Sci, Kumamoto 8600811, Japan
关键词
Hepatitis C; Natural killer cells; Subsets; IFN-gamma; CD107a; NATURAL-KILLER-CELLS; INTERFERON-ALPHA; VIRUS; CYTOTOXICITY; ACTIVATION; EXPRESSION; RECEPTORS; RIBAVIRIN; RESPONSES; CD81;
D O I
10.1016/j.bbrc.2010.02.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
impaired activity of NK (natural killer) cells has been proposed as a mechanism contributing to viral persistence and chronic infection in hepatitis C (HCV) infection. We aimed to assess the impact of HCV infection on NK cells regarding frequency, subset distribution, and cytotoxic and cytokine secretion functions, as well as IFN-alpha and ribavirin therapeutic effects on NK cells. Significant reduction of total NK frequency and the CD56(dim)16(+) subset was observed in chronic HCV patients. IFN-gamma expression upon stimulation with K562 was severely suppressed but cytotoxicity measured by CD107a expression was maintained. These adverse effects were reversed after treatment with pegylated IFN-alpha and ribavirin; however, these skewed functions were not recovered in treatment-resistant patients. Thus, HCV chronic infection severely affects NK functions, except for cytotoxicity. Altered NK cell frequency and cytokine secretion by HCV infection may contribute to impaired cellular immune response and virus persistence. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:331 / 337
页数:7
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