Abstract

Psoriasis is an autoimmune, chronic, inflammatory skin condition mediated by T cells. It differs from other inflammatory conditions by causing significant alterations in epidermal cell proliferation and differentiation that are both complicated and prominent. The lack of an appropriate animal model has significantly hindered studies into the pathogenic mechanisms of psoriasis since animals other than humans typically do not exhibit the complex phenotypic features of human psoriasis. A variety of methods, including spontaneous mutations, drug-induced mutations, genetically engineered animals, xenotransplantation models, and immunological reconstitution approaches, have all been employed to study specific characteristics in the pathogenesis of psoriasis. Although some of these approaches have been used for more than 50years and far more models have been introduced recently, they have surprisingly not yet undergone detailed validation. Despite their limitations, these models have shown a connection between keratinocyte hyperplasia, vascular hyperplasia, and a cell-mediated immune response in the skin. The xenotransplantation of diseased or unaffected human skin onto immune-compromised recipients has also significantly aided psoriasis research. This technique has been used in a variety of ways to investigate the function of T lymphocytes and other cells, including preclinical therapeutic studies. The design of pertinent in vivo and in vitro psoriasis models is currently of utmost concern and a crucial step toward its cure. This article outlines the general approach in the development of psoriasis-related animal models, aspects of some specific models, along with their strengths and limitations.

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