IL-23- and Imiquimod-Induced Models of Experimental Psoriasis in Mice.

Genome-wide association studies have found that polymorphisms in genes for IL-23 and its receptor are important in psoriasis, and blocking IL-23 is an effective therapy in the disease. The use of Aldara , a cream that contains the TLR7 and TLR8 agonist imiquimod (IMQ), was found to exacerbate psoriasis in some patients with pre-existing disease. Intradermal injections of IL-23 and topical application of Aldara/IMQ induce skin inflammation in mice with features similar to psoriasis-including epidermal hyperplasia and accumulation of inflammatory cells in epidermis and dermis-which is mediated by IL-17A, IL-22, and other factors implicated in the human disease.

Monocyte-derived inflammatory Langerhans cells and dermal dendritic cells mediate psoriasis-like inflammation.

Dendritic cells (DCs) have been implicated in the pathogenesis of psoriasis but the roles for specific DC subsets are not well defined. Here we show that DCs are required for psoriasis-like changes in mouse skin induced by the local injection of IL-23. However, Flt3L-dependent DCs and resident Langerhans cells are dispensable for the inflammation.