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

Antioxid Redox Signal. 2002 Jun;4(3):471-7. doi: 10.1089/15230860260196263.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

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

Substances

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