Editor's Summary

15 September 2005

What causes psoriasis

Psoriasis, a common inflammatory disease of skin and joints, has been variously regarded as an immune disorder that affects the skin (the inside-out hypothesis), or a skin disorder with immunological consequences (outside-in). In the absence of a good animal model it has been difficult to be certain. Now there is a good model. Starting from the discovery that epidermal keratinocytes in human psoriatic lesions have reduced expression of transcription factor JunB, Zenz et al. developed a mouse model in which epidermal deletion of JunB and c-Jun produces a condition almost identical to psoriasis. Genetic evidence shows that skin lesions develop independently of immune cells and that the arthritis is primarily mediated by TNF signalling. Immune cells seem to act merely as amplifiers of the inflammatory response. On the cover, human epidermis expressing JunB (stained red).

Article: Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins

Rainer Zenz, Robert Eferl, Lukas Kenner, Lore Florin, Lars Hummerich, Denis Mehic, Harald Scheuch, Peter Angel, Erwin Tschachler and Erwin F. Wagner

doi:10.1038/nature03963

Abstract | Full Text | PDF (805K) | Supplementary information