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British Medical Bulletin 2005 73-74(1):71-82; doi:10.1093/bmb/ldh051
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Published online 20 September 2005

© The Author 2005. Published by Oxford University Press on behalf of The British Council. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Immunological therapies for rheumatoid arthritis

Christopher J. Edwards

Department of Rheumatology, Southampton General Hospital, and MRC Epidemiology Resource Centre, University of Southampton, Southampton, UK

Correspondence to: Dr C. J. Edwards, Department of Rheumatology, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD. E-mail: cedwards{at}soton.ac.uk

Rheumatoid arthritis (RA) is a chronic inflammatory arthritis of the synovial joints that causes loss of function and a shortened life expectancy. In the last 10 years there have been major advances in the treatment of RA, including more aggressive use of disease-modifying anti-rheumatic drugs and the development of immune therapies targeted to molecules and cells important in the immunopathogenesis of RA. Molecular messengers that travel between cells (cytokines) have been found to be of major importance. Blocking the cytokine tumour necrosis factor {alpha} (TNF-{alpha}) produces significant improvement in RA, ankylosing spondylitis, psoriatic arthritis, psoriasis and Crohn’s disease. The use of cytokine blockers has shown the extent to which immune and inflammatory pathways are shared in a number of inflammatory diseases. There has also been an important proof of principle that blocking single cytokines can produce profound effects in inflammatory diseases.


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