ROS as signalling molecules in T cells - Evidence for abnormal redox signalling in the autoimmune disease, rheumatoid arthritis

Helen R. Griffiths*

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

Reactive oxygen species are recognised as important signalling molecules within cells of the immune system. This is, at least in part, due to the reversible activation of kinases, phosphatases and transcription factors by modification of critical thiol residues. However, in the chronic inflammatory disease rheumatoid arthritis, cells of the immune system are exposed to increased levels of oxidative stress and the T cell becomes refractory to growth and death stimuli. This contributes to the perpetuation of the immune response. As many of the effective therapies used in the treatment of rheumatoid arthritis modulate intracellular redox state, this raises the question of whether increased oxidative stress is causative of T-cell hyporesponsiveness. To address this hypothesis, this review considers the putative sources of ROS involved in normal intracellular signalling in T cells and the evidence in support of abnormal ROS fluxes contributing to T-cell hyporesponsiveness. © W. S. Maney & Son Ltd.

Original languageEnglish
Pages (from-to)273-280
Number of pages8
JournalRedox report
Volume10
Issue number6
DOIs
Publication statusPublished - Dec 2005

Keywords

  • immune response
  • reactive oxygen species
  • rheumatoid arthritis
  • ROS fluxes
  • T cells

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