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

Griffiths, Helen R.

doi:10.1179/135100005x83680

Cited by 103Redox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative MechanismsRheumatoid Arthritis Research and Therapies

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

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Griffiths, Helen R.·2005·Redox Report

DOI 10.1179/135100005x83680

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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.

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Rheumatoid arthritis is a disease whose aetiology is bound up with ROSs.
“One disease whose aetiology is well known to be bound up with ROSs is rheumatoid arthritis (RA) [36,1241-1246].”
From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [1246]

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Authors: Griffiths, H. R.
Affiliations: Aston University (GB)
Corresponding author: Griffiths, Helen R.
ORCID: Griffiths, Helen R.
Venue: Redox Report
Publisher: Informa UK Limited
Published: 2005-12
Volume: 10
Issue: 6
Pages: 273-280
ISSN: 1351-0002 (ISSN-L)
1743-2928
DOI: 10.1179/135100005x83680
OpenAlex: W1998727250
Cited by: 103
References: 67
Citations by year: 2026: 1 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 3 · 2020: 7 · 2019: 2 · 2018: 8 · 2017: 7 · 2016: 5 · 2015: 2 · 2014: 6 · 2013: 7 · 2012: 4
FWCI: 0.57
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Redox Report (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Keywords: reactive oxygen species, redox signaling, T cells, rheumatoid arthritis, oxidative stress, T cell hyporesponsiveness, thiol modification, transcription factor activation, chronic inflammation
MeSH terms: Antigens, Arthritis, Rheumatoid, Humans, Immune System, Models, Biological, Oxidation-Reduction, Phosphorylation, T-Lymphocytes, Apoptosis, Reactive Oxygen Species, Oxidative Stress

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

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