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Highly Accessed Editorial

A complicated liaison: IL-33 and IL-33R in arthritis pathogenesis

Thomas Kamradt* and Sebastian Drube

Author Affiliations

Institut für Immunologie, Universitätsklinikum Jena, Leutragraben 3, 07743 Jena, Germany

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Arthritis Research & Therapy 2013, 15:115  doi:10.1186/ar4209


See related research by Martin et al., http://arthritis-research.com/content/15/1/R13

Published: 2 May 2013

Abstract

Interruption of cytokine signaling, by targeting either the cytokine itself or its cellular receptor, is a mainstay in the therapy for patients with rheumatic diseases. Interleukin (IL)-33, a member of the IL-1 cytokine family, has emerged as an important mediator of inflammatory responses. In a side-by-side examination of IL-33-deficient and IL-33 receptor (IL-33R)-deficient mice in the K/BxN serum transfer model, arthritis was ameliorated in the IL-33R knockout (KO) mice but not in the IL-33 KO mice. These findings complement previous knowledge on IL-33R signaling, demonstrating that the IL-33R cross-activates other signaling pathways in addition to IL-33-mediated signals. The results reported by Martin and colleagues in a previous issue of Arthritis Research & Therapy underline the clinical relevance of IL-33R cross-signaling and further illustrate that targeting a cytokine receptor (IL-33R) can have completely different clinical outcomes than targeting the respective cytokine.