Understanding IFNλ in rheumatoid arthritis

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作者
Rik A de Groen
Bi-Sheng Liu
André Boonstra
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[1] University Medical Center Rotterdam,Department of Gastroenterology and Hepatology, Erasmus MC
[2] Leiden University Medical Center,Department of Rheumatology
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Unraveling the mechanisms underlying the inflammatory response in rheumatoid arthritis is crucial in order to better understand the disease and to develop novel therapeutic approaches. Although the effect of type I interferons on fibroblasts and in the context of rheumatoid arthritis has been described for some time, little is known on the effects of the type III interferons, also known as IFNλ. In a previous issue, Xu and colleagues demonstrate that one of the members of the IFNλ family, IFNλ1, enhances Toll-like receptor expression and consequently promotes the production of proinflammatory cytokines known to be involved in initiating and maintaining the inflammatory responses in rheumatoid arthritis.
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