Psoriasis is a skin disease mainly developed in humans, although it is also seen in monkeys and dogs. Animal models with psoriasis-like lesions have been a key factor for its understanding. Xenotransplants of human psoriatic skin in immunodeficient mice were the first approach for the association of immunologic problems with the development of psoriasis and have been also useful for the evaluation on new therapeutic agents. Imiquimod-induced murine psoriasis is nowadays one of the most used animal models to study this disease, perhaps because healthy wild-type mice are used, which means that it is an affordable model, easy to generate, and, more importantly, resembles the inflammatory, angiogenic and hyperproliferative characteristics of human psoriasis. Several transgenic (over-expressing VEGF, Tie2, TGFβ, STAT3, IL-36, PPARβ/γ) and knockout (lacking IκBα, JunB, IFNR-2, IL-36RA, CD18, IKK2) mice have been useful for the association of specific molecules for the development of psoriasis. Other approach has been the use of both transgenic/knockout mice and imiquimod treatment, where the importance of βTrCP, IκBζ, IL-35 and Tnip1 for the development of psoriasis was found. In this chapter, some of these animal models are discussed.
Part of the book: Psoriasis