Article
TNF α inhibitors in the treatment of non-infectious uveitis
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Published: | September 22, 2004 |
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Tumour necrosis factor (TNF) α is produced by various cell populations of the immune system. During inflammation, TNFα can activate T lymphocytes and macrophages through ligation of the receptors p55 (TNFr1) and p75 (TNFr2) and induces production of other pro-inflammatory cytokines. Elevated concentrations of TNFα in the eyes of patients with active uveitis and experimental data from animal models suggest an important role of this cytokine in the pathogeneses of anterior and posterior uveitis. Targeting TNFα therefore appears to be a promising strategy for the treatment of non-infectious uveitis.
Two TNFα inhibitors are currently approved for the treatment of rheumatoid arthritis and Crohns disease. Infliximab is a chimeric IgG antibody directed against TNFα. Etanercept is a fusion protein of the Fc part of human IgG and TNFr2. The longterm use of these two agents provided abundant data about side effects. Various studies evaluated the efficacy of infliximab and etanercept for the treatment of anterior and posterior uveitis. A recent phase I/II trial investigated a new TNFr1 fusion protein for the treatment of posterior uveitis. This presentation summarizes the results of these studies and discusses the current role of TNFα inhibitors in the treatment of non-infectious uveitis.