Animal models of Psoriasis - What can we learn from them?

Research into the pathogenesis of psoriasis has been hampered by the lack o f an animal disease resembling this common human skin disorder. Over the pa st few years, however, various rodent models that mirror aspects of the pso riatic phenotype and pathogenesis have become available. Here, the most pro minent models are compared with human psoriasis and potential uses for psor iasis research are reviewed. Asebia tab), flaky skin (fsn), and chronic pro liferative dermatitis (cpd) are spontaneous mouse mutations with psoriasifo rm skin alterations of unclear pathogenesis. Transgenic mice with cutaneous overexpression of cytokines, such as interferon-gamma, interleukin-1 alpha , keratinocyte growth factor, transforming growth factor-alpha, interferon- 6, vascular endothelial growth factor, or bone morphogenic protein-6, are v aluable tools for studying in vivo effects of individual cytokines in the p athogenesis of psoriasiform features. Psoriasiform lesions also were seen i n beta(2)-integrin hypomorphic mice backcrossed to the PL/J strain and in b eta(1)-integrin transgenic mice. A T cell-based immunopathogenesis of psori asiform features was shown in a form of graft versus-host disease in scid/s cid mice reconstituted with CD4(+)/CD45RB(hi) T lymphocytes as well as in H LA-B27/h beta(2)m transgenic rats, demonstrating that dysregulated T cells can induce psoriasiform skin alterations without a primary epithelial abnor mality. Finally, xenotransplantation models using human skin grafted on to immunodeficient mice are attractive, as different cell types and some envir onmental factors leading to psoriasiform features may be studied in human t issue, Overall, although there is no animal model imitating psoriasis compl etely, many aspects of this common human skin disorder are mirrored in the currently available models and psoriatic plaques can be created in xenotran splantation models.