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Annals of the Rheumatic Diseases 2009;68:157-158; doi:10.1136/ard.2008.097899
Copyright © 2009 BMJ Publishing Group Ltd & European League Against Rheumatism.

EDITORIAL

Interferon β for rheumatoid arthritis: new clothes for an old kid on the block

Margriet J Vervoordeldonk1,2, Caroline J Aalbers1,2, Paul P Tak1,2

1 Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
2 Arthrogen BV, Amsterdam, The Netherlands

Correspondence to:
Professor P P Tak, Division of Clinical Immunology and Rheumatology, F4-218, Academic Medical Center/University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands; p.p.tak@amc.uva.nl

Accepted 23 September 2008

The first 150 words of the full text of this article appear below.

The type I interferons (IFNs), IFNβ and various IFN{alpha}s, are pleiotropic cytokines acting on a range of cell types and eliciting a diverse range of responses. For many years IFNβ was thought to be a potential agent for the treatment of a variety of immune-mediated diseases. Clinical trials showing a beneficial effect of IFNβ treatment on clinical and MRI measures in relapsing–remitting multiple sclerosis were published almost a decade ago.1 2 These publications have stimulated studies on its potential for the treatment of patients with rheumatoid arthritis (RA). IFNβ has clear anti-inflammatory properties3 and plays an important role in bone homeostasis.4 Of special interest is the ability of IFNβ to reduce the secretion of proinflammatory mediators such as interleukin (IL)6, tumour necrosis factor (TNF){alpha}, matrix metalloproteinases (MMPs) and prostaglandin E2, which are key players in the pathogenesis of RA.5 6 In addition, IFNβ has antiangiogenic properties,7 which could boost therapeutic . . . [Full text of this article]


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