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. 2016 Jan 15;23(6):1073–1085. doi: 10.1038/cdd.2015.162

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Copyright © 2016 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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Functional interplay between ΔNp63 and immune activation, itch and defects in keratinocyte terminal differentiation in AD. This model depicts the role ΔNp63 plays in directing various components involved in the development of atopic dermatitis. Elevated expression levels of ΔNp63 results in direct activation of IL-33 signaling and subsequent Th2 polarization. Induction of pruritus occurs through direct regulation of IL-31, IL-31ra and OSMR gene expression. Elevated ΔNp63 epidermal expression, scratching response to pruritus and Th2 cell activation all contribute to alterations in keratinocyte terminal differentiation