Psoriasis is an immune-mediated inflammatory skin disease characterized by skin thickening, red plaques and dry scales. Psoriasis can be triggered by many factors, including injury, trauma, infection and medications. The disease is assessed clinically using the Psoriasis Activity and Severity Index (PASI) scale which ranks severity of erythema (redness), induration (thickness) and desquamation (scale). Histologically, the disease is characterized by epidermal thickening due to hyperkeratosis, infiltration of immune cells in dermis and epidermis, parakeratosis and neovascularization. A hallmark of the disease in humans is the involvement of IL-23/IL17 cytokine axis.
Charles River has characterized a clinically relevant model of psoriasis in mice through the topical application of 5% imiquimod (IMQ) cream. This IMQ-induced psoriasis models human plaque-type psoriasis in which the IL-23/IL-17 cytokine axis plays a pivotal role.
Study parameters include in-life clinical evaluation of skin, histopathological evaluation of skin sections and optional cytokine analysis in skin and/or internal immune organs.
Imiquimod-induced psoriasis-like skin inflammation in mice is mediated via the IL-23/IL-17 axis. Journal of Immunology, 2009. 182(9):5836-45.
Immunology of psoriasis. Annual Review of Immunology, 2014. 32:227-55.