Redox events in HTLV-1 Tax-induced apoptotic T-cell death.
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 1 (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.
Chlichlia
Katerina
K
Division of Cellular Immunology (G0100), Tumor Immunology Program, German Cancer Research Center, Im Neuenheimer Feld 280, D69120 Heidelberg, Germany. katerina.chlichlia@urz.uni-heidelberg.de
Los
Marek
M
Schulze-Osthoff
Klaus
K
Gazzolo
Louis
L
Schirrmacher
Volker
V
Khazaie
Khashayarsha
K
D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology*; D002471:Cell Transformation, Neoplastic; D016356:Gene Products, tax / Q000378:metabolism*; D015368:Human T-lymphotropic virus 1; D006801:Humans; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D016328:NF-kappa B / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011948:Receptors, Antigen, T-Cell; D013601:T-Lymphocytes / Q000502:physiology*
D000975:Antioxidants; D016356:Gene Products, tax; D016328:NF-kappa B; D011948:Receptors, Antigen, T-Cell