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Journal of Biomedicine and Biotechnology
Volume 2012, Article ID 147413, 5 pages
Review Article

Ustekinumab in Psoriasis Immunopathology with Emphasis on the Th17-IL23 Axis: A Primer

1Department of Dermatopathology, University Hospital of Liège, 4000 Liège, Belgium
2Faculty of Medicine, University of Franche-Comté, 25000 Besançon, France
3Department of Dermatology, University Hospital of Besançon, 25000 Besançon, France
4Inserm Research Unit U645, IFR133, 25000 Besançon, France

Received 31 January 2012; Revised 5 March 2012; Accepted 5 March 2012

Academic Editor: Enzo Berardesca

Copyright © 2012 Pascale Quatresooz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Psoriasis is a chronic relapsing immunoinflammatory dermatosis that is commonly associated with systemic comorbidities. The pathogenic importance of interleukin (IL)-12 and IL-23 is beyond doubt, as well as the involvement of T helper cells (Th)1 and Th17 cells. There is upregulation of the p40 subunit shared by IL-12 and IL-23 and of the IL-23 p19 subunit, but not an increased expression of the IL-12 p35 subunit. This indicates that IL-23 appears more involved than IL-12 in the pathogenesis of psoriatic plaques. Ustekinumab is a fully human monoclonal antibody of the immunoglobulin (Ig) G1 class targeting the p40 subunit common to both IL-12 and IL-23, thus inhibiting both IL-12 and IL-23 receptor-mediated signalling. Ustekinumab is part of the recent biologic therapies active in psoriasis, autoimmune arthritides, and inflammatory bowel diseases.