Psoriasis is a chronic inflammatory skin disease with a prevalence of 2–3 %. It appears to result from a combination of genetic and environmental factors, but the precise pathogenesis is still unknown. Neurogenic inflammation is involved in psoriasis pathogenesis as well, but the role of neurogenic factors is currently unclear. Molecular studies often involve material obtained from patients. However, many questions and especially experimental manipulations are not suited for study in humans. Imiquimod application on mouse skin leads to immune cell infiltration, inflammation with intense redness, epidermal thickening, and scaling that jointly greatly resembles human psoriasis. Here we describe the use of surgical denervation in the imiquimod-induced psoriasiform model, to study the role of skin innervation and neuropeptides in the pathogenesis of psoriasis.

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Keywords (γδ) T cells, Denervation, IL-17, IL-23, Imiquimod, Mouse model, Nerves, Neuropeptides, Psoriasis, TLR7
Persistent URL dx.doi.org/10.1007/978-1-4939-6786-5_6, hdl.handle.net/1765/95553
Citation
Onderdijk, A.J, Hekking-Weijma, J.M, Florencia, E, & Prens, E.P. (2017). Surgical denervation in the imiquimod-induced psoriasiform mouse model. In Björn E. Clausen, Jon D. Laman (2017) Inflammation : Methods and Protocols (pp. 75–81). doi:10.1007/978-1-4939-6786-5_6