Journal article

Publication year: 2010

Pages: 246-251

Journal: Current Opinion in Rheumatology

Volume number: 22

Issue number: 3

ISSN: 1040-8711

eISSN: 1531-6963

DOI Link: https://doi.org/10.1097/BOR.0b013e3283373fa0

Publisher: Lippincott, Williams & Wilkins

Abstract: 

Purpose of review

Several studies have evaluated the efficacy and safety of novel therapeutic options targeting interleukin-1 (IL-1), which not only plays a significant role in rheumatoid arthritis, but also in other rheumatic diseases, for which only limited therapeutical options exist.

Recent findings

Three different strategies have been pursued and evaluated in the past years: preventing IL-1 binding by occupying IL-1 receptors with anakinra, an imitation of the naturally occurring IL-1 receptor antagonist, anakinra; development of the fully human monoclonal anti-IL-1 beta antibody canakinumab; and synthesis of the dimeric fusion protein rilonacept, consisting of the ligand-binding domain of interleukin-1 receptor type I and its accessory protein, bound to human IgG1. Each of these three anti-IL-1 agents proved efficacy in distinct clinical situations and disease entities.

Summary

Owing to the observation that IL-1 is not only involved in signaling processes resulting in autoimmune and crystal-induced joint destruction but also in several hereditary autoinflammatory syndromes, its value both in pathophysiology as well as for novel advances in medication has significantly improved in the past years leading to an enrichment of the current therapeutic armamentarium for the affected patients.

Harvard Citation style: Geyer, M. and Mueller-Ladner, U. (2010) Actual status of antiinterleukin-1 therapies in rheumatic diseases, Current Opinion in Rheumatology, 22(3), pp. 246-251. https://doi.org/10.1097/BOR.0b013e3283373fa0

APA Citation style: Geyer, M., & Mueller-Ladner, U. (2010). Actual status of antiinterleukin-1 therapies in rheumatic diseases. Current Opinion in Rheumatology. 22(3), 246-251. https://doi.org/10.1097/BOR.0b013e3283373fa0