Redox events in HTLV-1 Tax-induced apoptotic T-cell death.

Abstract

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.

• Authors: Katerina Chlichlia, Marek Los, Klaus Schulze-Osthoff, Louis Gazzolo, Volker Schirrmacher, Khashayarsha Khazaie
• Journal: Antioxidants & redox signaling (Antioxid Redox Signal) Vol. 4 Issue 3 Pg. 471-7 (Jun 2002) ISSN: 1523-0864 [Print] United States
• PMID: 12215214 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Antioxidants
• Gene Products, tax
• NF-kappa B
• Receptors, Antigen, T-Cell

Topics

• Antioxidants (metabolism)
• Apoptosis (physiology)
• Cell Transformation, Neoplastic
• Gene Products, tax (metabolism)
• Human T-lymphotropic virus 1
• Humans
• Leukemia-Lymphoma, Adult T-Cell (etiology, metabolism, physiopathology)
• NF-kappa B (metabolism)
• Oxidation-Reduction
• Oxidative Stress
• Receptors, Antigen, T-Cell
• T-Lymphocytes (physiology)