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The type I interferons (IFNs), IFNβ and various IFNαs, 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)α, 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 effect in RA.8
The notion that IFNβ treatment may reduce arthritis is supported by animal experiments. Several studies examining the effect of IFNβ in collagen-induced arthritis (CIA) in mice have been published. In one study mice were given daily intraperitoneal injections with mouse IFNβ9 and in another study, mice were injected intraperitoneally with a single injection of fibroblasts expressing IFNβ, resulting in continuous IFNβ production.10 Both studies revealed a beneficial effect on arthritis activity and histological scores for inflammation. A similar effect was shown in CIA in rhesus monkeys that were treated daily …
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