1. ¹Department of Dermatology, University of Michigan Medical Center, Ann Arbor, Michigan, USA
2. ²Department of Immunology, Landspitali University Hospital, Reykjavik, Iceland
3. ³Unit for Laboratory Animal Medicine, Animal Research Facility, University of Michigan, Ann Arbor, Michigan, USA
4. ⁴Department of Radiation Oncology, University of Michigan Medical Center, Ann Arbor, Michigan, USA
5. ⁵Ann Arbor Veterans Affairs Health System, Ann Arbor, Michigan, USA

Correspondence: Dr Johann E. Gudjonsson, Department of Dermatology, 1910 Taubman Center, 1500 E. Medical Center Drive, University of Michigan, Ann Arbor, Michigan 48109, USA. E-mail: johanng@med.umich.edu

Received 15 February 2006; Revised 21 December 2006; Accepted 26 December 2006; Published online 12 April 2007.

Abstract

Psoriasis is a T-cell-mediated chronic inflammatory skin disease believed to be of autoimmune nature that can be triggered or worsened by streptococcal throat infections. In addition to conventional chronic inflammatory changes, psoriasis is characterized by complex and striking alterations in epidermal growth and differentiation. Psoriasis is generally not observed in animals other than man, and this lack of a suitable animal model has greatly hindered research into the pathogenesis of psoriasis. Multiple transgenic, knockout, and reconstituted models of psoriasis have been developed over the past two decades. Despite their limitations, these models have demonstrated that keratinocyte hyperplasia, vascular hyperplasia, and cell-mediated immunity in the skin are closely interrelated. Xenograft models, in which involved and uninvolved psoriatic skin are transplanted onto immunodeficient mice, are the only models that come close to incorporating the complete genetic, immunologic, and phenotypic changes of the disease. They have shown conclusively that psoriasis is a T-cell-mediated disease, and have been used to elucidate novel pathogenic pathways. In this review, we describe various animal models, detail the immunologic and intracellular pathways that mediate these phenotypes and assess the utility of these models to better understand this disease.