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Published in: BioDrugs 6/2014

01-12-2014 | Review Article

The Role of Interleukin-17A in Psoriatic Disease

Authors: Silvano Adami, Andrea Cavani, Francesco Rossi, Giampiero Girolomoni

Published in: BioDrugs | Issue 6/2014

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Abstract

The pathogenic mechanisms of specific immune-mediated inflammatory diseases (IMIDs) are not fully understood, but are thought to involve activated T cells with the release of pro-inflammatory cytokines. Understanding the autoimmune inflammatory pathways has led to the development of biological agents that target specific components of effector immune mechanisms. Despite the availability of many effective drugs, a large proportion of patients with moderate to severe IMID do not receive adequate treatment, and many therapies show decreased efficacy over time. Therefore, there is a need for new therapies. One subset of T helper cells, Th17, and the cytokine interleukin-17 (IL-17) play a central role in the pathophysiology of autoimmune diseases such as psoriasis. IL-17 is involved in the modulation of pro-inflammatory cytokines, haematopoietic growth factors, antimicrobial peptides, chemokines, and molecules involved in tissue remodelling; the inflammatory cascades triggered by Th17 cells and IL-17 itself, when unregulated, can result in widespread inflammation-related damage. Evidence of increased Th17 activity and high levels of IL-17 has been found in psoriasis, as well as other inflammatory conditions, thereby signalling the potential utility of IL-17 as a therapeutic target. Clinical trials investigating IL-17 inhibitors, such as secukinumab, in patients with psoriatic disease have reported no significant safety concerns so far. It is hoped that these agents will improve the long-term prognosis of patients with these debilitating disorders.
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Metadata
Title
The Role of Interleukin-17A in Psoriatic Disease
Authors
Silvano Adami
Andrea Cavani
Francesco Rossi
Giampiero Girolomoni
Publication date
01-12-2014
Publisher
Springer International Publishing
Published in
BioDrugs / Issue 6/2014
Print ISSN: 1173-8804
Electronic ISSN: 1179-190X
DOI
https://doi.org/10.1007/s40259-014-0098-x

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Acknowledgement to Referees

Acknowledgement to Referees