Rheumatology Advance Access originally published online on August 10, 2004
Rheumatology 2004 43(11):1337-1345; doi:10.1093/rheumatology/keh333
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Rheumatology Vol. 43 No. 11 © British Society for Rheumatology 2004; all rights reserved
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Corticosteroid resistance in rheumatoid arthritis: molecular and cellular perspectives
1 Bone and Joint Research Unit, Barts and The London, Queen Mary School of Medicine and Dentistry, University of London, Charterhouse Square, London EC1M 6BQ, UK and 2 Department of Biochemistry, School of Medicine, Adnan Menderes University, Turkey.
Correspondence to: I. C. Chikanza, Bone and Joint Research Unit, Barts and The London, Queen Mary School of Medicine & Dentistry, University of London, Charterhouse Square, London EC1M 6BQ, UK. E-mail: icchikanza@qmul.ac.uk
KEY WORDS: Corticosteroid resistance, Rheumatoid arthritis, Corticosteroids, Corticosteroid receptor, Cytokines, Inflammation
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Introduction |
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Corticosteroids are often used to treat a range of chronic autoimmune inflammatory diseases such as asthma, inflammatory bowel disease and rheumatoid arthritis (RA). RA is the most prevalent autoimmune chronic inflammatory rheumatic disorder with a prevalence of 1% in developed nations. It is more common in women than men, suggesting that perturbations of the hormonal systems may be involved in disease pathophysiology. The aetiology of the disease is unknown, but the physiological mechanisms of inflammation involved in this disease share common pathways with other inflammatory situations [1, 2]. However, the reasons why inflammation persists in RA remain unknown but might relate in part to a dysregulation of the interactions between neuroendocrine and immune systems at the onset of acute inflammation [2–6]. Acute inflammation can be initiated by a number of inflammatory triggers. This results in a programmed sequence of physiological mechanisms which begin with the
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The molecular basis of the biological activity of corticosteroids |
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The physiological regulation of corticosteroid effects |
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Modulation of corticosteroid bioavailability and bioactivity
Cytokines as physiological regulators of corticosteroids
Hypothalamic–pituitary-mediated regulation of corticosteroid bioactivity
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What are the mechanisms of corticosteroid resistance? |
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Polymorphic and genetic variations of the corticosteroid receptor
The expression of the corticosteroid receptor isoforms
The phosphorylation status of the corticosteroid receptor
Cross-talk between transcription factors: alterations in intracellular signalling mechanisms
Perturbations of the cytokine milieu in RA
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Conclusions |
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