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Editorial

Understanding IFNλ in rheumatoid arthritis

Rik A de Groen1, Bi-Sheng Liu2 and André Boonstra1*

Author Affiliations

1 Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center Rotterdam, ‘s-Gravendijkwal 230, Room Na-1011, 3015 CE, Rotterdam, the Netherlands

2 Department of Rheumatology, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, the Netherlands

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Arthritis Research & Therapy 2014, 16:102  doi:10.1186/ar4445


See related research by Xu et al., http://arthritis-research.com/content/15/5/R170

Published: 21 January 2014

Abstract

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.