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Craig A. Elmets, MD

Arch Dermatol. 2006;142:1499-1500.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Psoriasis-Like Skin Disease and Arthritis Caused by Inducible Epidermal Deletion of Jun Proteins
Zenz R, Eferl R, Kenner L, et al
Nature. 2005;437:369-375

Psoriasis is a frequent, inflammatory disease of skin and joints with considerable morbidity. Here we report that in psoriatic lesions, epidermal keratinocytes have decreased expression of JunB, a gene localized in the psoriasis susceptibility region PSORS6. Likewise, inducible epidermal deletion of JunB and its functional companion c-Jun in adult mice leads (within two weeks) to a phenotype resembling the histological and molecular hallmarks of psoriasis, including arthritic lesions. In contrast to the skin phenotype, the development of arthritic lesions requires T and B cells and signalling through tumour necrosis factor receptor 1 (TNFR1). Prior to the disease onset, two chemotactic proteins (S100A8 and S100A9) previously mapped to the psoriasis susceptibility region PSORS4, are strongly induced in mutant keratinocytes in . . . [Full Text of this Article]

COMMENT

AUTHOR INFORMATION

Department of Dermatology, University of Alabama at Birmingham

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