Psoriasis

Introduction

Psoriasis (Ps) is a chronic inflammatory skin disease affecting about 2–3% of the worldwide population. Ps is characterized by infiltration of immune cells, epidermal hyperproliferation, and abnormal keratinocyte differentiation. The pathogenesis of psoriasis is multifactorial, with genetic, environmental, and immunological factors contributing to the phenotypes. Psoriasis involves excessive proliferation and altered differentiation of epidermal keratinocytes, likely mediated by the immune system. Genetic alterations that affect the key signaling pathways involved in inflammatory immune responses in keratinocytes and inflammatory cells can alter skin homeostasis and induce psoriasis.

Animal Model

For psoriasis research, there are several categories of experimental animal models, spontaneous, genetically engineered (both transgenic and knockout), xenotransplantation, and direct induced, among which the “direct induced” type is most feasible for industrial drug development and screening.

Imiquimod (IMQ) induced Ps model

Imiquimod (IMQ) is a ligand for Toll-like receptors 7/8 which activates macrophages, monocytes and dendritic cells, by directly administrating on mice skin, it induces significant psoriasis-like skin damage, IMQ-model is commonly developed in both C57BL/6 and BALB/c mice.

IL-23 induced Ps model

IL-23 stimulates and promotes the differentiation of Th17 cells, the development of Th17 cells and the production of cytokines such as IL-17A. Localized psoriasis-like lesions are induced by direct injection of IL-23 into the skin of the mouse ear, resulting in pathological features similar to those of human psoriasis.

Examples

Key signals in psoriasis (Ps) development

Characterization and Evaluation of Optimized IMQ-induced Psoriasis Model. (a) Graphic time-line of modelling. (b) Upper, typical PASI scoring plot for disease progression; lower, individual scoring for scaling formation, redness and thickness. (c) Representative images of back skin damage. (d) Bodyweight change. (e) Skin thickness change. (f) Representative Hematoxylin-Erosin (H&E) staining of mice skin. (g) Representative image of skin damage. ^#1, ^#2 and ^#3 represents three individual experiment, respectively. ^*P < 0.05, ^***P < 0.001, comparing to model group, Anti-IL17A, Anti-IL17A antibody; Dex, Dexamethasone.

References

[1] Bocheńska Katarzyna, Smolińska Elwira, Moskot Marta, et al. Models in the Research Process of Psoriasis[J]. Int J Mol Sci, 2017, 18 (12). doi:10.3390/ijms18122514

[2]Li Qingran, Liu Weiping, Gao Shidong, et al. Application of imiquimod-induced murine psoriasis model in evaluating interleukin-17A antagonist[J]. BMC Immunol, 2021, 22 (1): 11. doi:10.1186/s12865-021-00401-3