Redox events in HTLV-1 tax-induced apoptotic T-cell death

被引:18
作者
Chlichlia, K
Los, M
Schulze-Osthoff, L
Gazzolo, L
Schirrmacher, V
Khazaie, K
机构
[1] German Canc Res Ctr, Div Cellular Immunol G0100, Tumor Immunol Program, D-69120 Heidelberg, Germany
[2] Univ Munster, Dept Immunol & Cell Biol, D-48149 Munster, Germany
[3] Ecole Normale Super Lyon, INSERM U412, F-69367 Lyon 07, France
[4] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA
关键词
D O I
10.1089/15230860260196263
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
A number of studies implicate reactive oxygen intermediates in the induction of DNA damage and apoptosis. Recent studies suggest that the human T-cell leukemia virus type I (HTLV-1) Tax protein induces oxidative stress and apoptotic T-cell death. Activation of the T-cell receptor/CD3 pathway enhances the Tax-mediated oxidative and apoptotic effects. Tax-mediated apoptosis and oxidative stress as well as activation of nuclear factor-kappaB can be potently suppressed by antioxidants. This review focuses on Tax-dependent changes in the intracellular redox status and their role in Tax-mediated DNA damage and apoptosis. The relevance of these observations to HTLV-1 virus-mediated T-cell transformation and leukemogenesis are discussed.
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收藏
页码:471 / 477
页数:7
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