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ROS as signalling molecules in T cells – evidence for abnormal redox signalling in the autoimmune disease, rheumatoid arthritis
Open accessAbstract
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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“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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Metadata
- 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
- 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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