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Interleukin-20 plays a critical role in maintenance and development of psoriasis in the human xenograft transplantation model.

Authors :
Stenderup, K.
Rosada, C.
Worsaae, A.
Dagnaes-Hansen, F.
Steiniche, T.
Hasselager, E.
Iversen, L. F.
Zahn, S.
Wöldike, H.
Holmberg, H. Lindgreen
Rømer, J.
Kragballe, K.
Clausen, J. T.
Dam, T. N.
Source :
British Journal of Dermatology; Feb2009, Vol. 160 Issue 2, p284-296, 13p, 1 Diagram, 1 Chart, 6 Graphs
Publication Year :
2009

Abstract

Background Interleukin (IL)-20 is a recently discovered cytokine displaying increased levels in psoriatic lesions. Interestingly, IL-20 levels decrease with antipsoriatic treatment, correlating with clinical improvement. However, the role of IL-20 in the aetiology of psoriasis is unknown. Objectives In this study, we investigate the effects both of blocking IL-20 signalling in psoriatic plaques and of adding IL-20 to nonlesional psoriasis skin. Methods We employed the human skin xenograft transplantation model in which psoriatic plaques and nonlesional keratome skin biopsies obtained from donors with moderate to severe plaque psoriasis were transplanted on to immuno-deficient mice. The transplanted mice were treated with anti-IL-20 antibodies or recombinant human IL-20. Results We demonstrate that blocking IL-20 signalling with anti-IL-20 antibodies induces psoriasis resolution and inhibits psoriasis induction. We also demonstrate that continuous IL-20 infusion, together with injection of additional nonactivated leucocytes, promotes induction of psoriasis in nonlesional skin from patients with psoriasis. Conclusions The results suggest that IL-20 plays a critical role in the induction and maintenance of psoriasis, and IL-20 is suggested as a new possible specific target in psoriasis treatment. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00070963
Volume :
160
Issue :
2
Database :
Complementary Index
Journal :
British Journal of Dermatology
Publication Type :
Academic Journal
Accession number :
36143454
Full Text :
https://doi.org/10.1111/j.1365-2133.2008.08890.x