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Mouse Model Of Human Psoriasis

ScienceDaily (Mar. 29, 2009) — Researchers led by Nicole Ward at Case Western Reserve University, Cleveland have developed a new mouse model to study human psoriasis.

These findings are presented in the April 2009 issue of The American Journal of Pathology.

Psoriasis is a chronic inflammatory disease that causes red scaly patches to appear on the skin. It is characterized by excessive skin production, formation of new blood vessels, and the presence of white blood cells. Study of psoriasis has been limited, however, due to the absence of a mouse model that adequately reproduces these symptoms.

Over-expression Tie-2, a molecule involved in the formation of new blood vessels, in two types of skin cells, epithelial cells and keratinocytes, has provided the best psoriasis model to date. To determine whether Tie-2 over-expression in epithelial cells or keratinocytes resulted in the psoriasis phenotype, Wolfram et al engineered two new mouse models in which Tie-2 expression was limited to either epithelial cells or keratinocytes. Only the keratinocyte-restricted Tie-2 mice developed symptoms similar to human psoriasis. These symptoms were reduced by treatment with cyclosporin A, a common psoriasis therapy. Keratinocyte-restricted Tie-2 mice, therefore, may serve as an animal model for human psoriasis.

The psoriasis model developed by Dr. Ward's group "bears a striking resemblance to human psoriasis, meeting multiple criteria at the clinical, histological, biochemical, immunophenotype, and pharmacologic levels … and therefore will become important for studying pathological mechanisms of psoriasis and pre-clinical testing of new therapeutics."


Journal reference:

  1. Wolfram JA, Diaconu D, Hatala DA, Rastegar J, Knutsen DA, Lowther A, Askew D, Gilliam AC, McCormick TS, Ward NL. Keratinocyte but not endothelial cell specific over-expression of Tie-2 leads to the development of psoriasis. Am J Pathol, 2009; 174: 1443-1458
Adapted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
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