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General approaches to generate animal models of psoriasis, features of some specific models, their value for psoriasis research, and their use for drug development are discussed in this article.
Fully animal models of psoriasis have nonetheless not only shed light on the biological functions of given inflammatory mediators or other molecules but also tremendously contributed to the discussion on central pathogenic questions, such as the roles of innate and adaptive immune mechanisms, keratinocytes, and endothelial cells in psoriasis.
Additionally, the approach used in this paper provides an objective and quantitative method for evaluation of proposed mouse models of psoriasis, which can be strategically applied in future studies to score strengths of mouse phenotypes relative to specific aspects of human psoriasis.
For this we studied different models of psoriasis, such as the imiquimod-induced psoriasis-like skin inflammation in mice [22] and ex vivo-stimulated human skin explants, and investigated GATA3 expression and activation in keratinocytes during epidermal regeneration, which is known to share many characteristics with psoriatic skin inflammation [23].
These analyses provide the first transcriptomics-based assessment of correspondence between human psoriasis and multiple mouse phenotypes, and we suggest that similar analytic strategies can be adopted in future work to evaluate existing and new mouse models of psoriasis and other skin diseases.
The first models of psoriasis were spontaneous mutations in mice which exhibited a psoriasis-like phenotype.
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In a transgenic mouse model of psoriasis, NVP-BAW2881 reduced the number of blood and lymphatic vessels and infiltrating leukocytes in the skin, and normalized the epidermal architecture.
The present study was designed to characterize the potential therapeutic effects of DZ2002 on murine model of psoriasis and reveal the correlated mechanisms.
Psoriasis is a T-cell-mediated skin disease with autoimmune nature that is generally not observed in animals, this lack of a relevant experimental animal model of psoriasis has hindered the investigation of pathogenesis of disease.
In a mouse model of psoriasis induced by topical application of Imiquimod, it was found that ILC3s are a cellular source of IL-17A and IL-22 that mediate the Imiquimod-induced psoriasis-like disease (Pantelyushin et al., 2012).
We employed an imiquimod (IMQ -induced murIMQ -induced psoriasis, in which Th17 cytokines like IL-23 and IL-17 were highly involved (van der Fits et al., 2009; Imurine al., 2015).
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