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Rabeony, H., Pohin, M., Vasseur, P., Petit-Paris, I., Jegou, J.F., Favot, L., Frouin, E., Boutet, M.A., Blanchard, F., Togbe, D., Ryffel, B., Bernard, F.X., Lecron, J.C. and Morel, F. (2015) IMQ-Induced Skin Inflammation in Mice Is Dependent on IL-1R1 and MyD88 Signaling But Independent of the NLRP3 Inflammasome. European Journal of Immunology, 45, 2847-2857.
https://doi.org/10.1002/eji.201445215

has been cited by the following article:

• TITLE: Expression of Skin Barrier Protein Filaggrin in Skin Diseases without Atopic Dermatitis

  AUTHORS: Yang Zhang, Chen Tu, Shuang Wang, Shengxiang Xiao

  KEYWORDS: Skin Barrier, Psoriasis, Filaggrin, Atopic Dermatits

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.6 No.1, January 29, 2018

  ABSTRACT: The epidermis represents an essential barrier versus a broad range of exogenous stimuli. To form a functional epidermis, keratinocytes express filaggrin which plays a vital role in atopic dermatitis. However the relationship between filaggrin and other skin diseases remains unknown. In our study we chose 5 different common skin diseases and analyzed the expression of filaggrin in the skin using immunohistochemistry. Imiquimod (IMQ)-induced mouse model was used for detecting the filaggrin level and barrier function. The results indicated that the expression of filaggrin is reduced in psoriasis compared to the other skin diseases. Furthermore in vivo study showed that the skin barrier is defected with a decreased expression of filaggrin in IMQ-induced psoriasis mouse model, which is accompanied with an increased level of IL-17/IL-23. In conclusion, the defective skin barrier is involved in the development of psoriasis in human and mice with a reduced expression of filaggrin which may be regulated by the increased level of IL-17/IL-23 in the skin.