IL-4 regulates skin homeostasis and the predisposition toward allergic skin inflammation.

Abstract	IL-4 promotes the development of Th2 cells and allergic inflammation. In atopic dermatitis lesions, IL-4 decreases the expression of multiple genes associated with innate defense, including genes in the epidermal differentiation complex (EDC) that regulate epidermal barrier function. However, it is not clear whether IL-4 also contributes to homeostatic control of EDC genes. In this report, we demonstrate that expression of EDC genes and barrier function is increased in the absence of endogenous IL-4. Mice that express a constitutively active Stat6 (Stat6VT) are prone to the development of allergic skin inflammation and have decreased expression of EDC genes. IL-4 deficiency protects Stat6VT transgenic mice from the development of allergic skin inflammation and decreased recovery time in barrier function following skin irritation, with a concomitant increase in EDC gene expression. These data suggest that IL-4 plays an important role in regulating epidermal homeostasis and innate barrier function.
Authors	Sarita Sehra, Yongxue Yao, Michael D Howell, Evelyn T Nguyen, Geoffrey S Kansas, Donald Y M Leung, Jeffrey B Travers, Mark H Kaplan
Journal	Journal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 184 Issue 6 Pg. 3186-90 (Mar 15 2010) ISSN: 1550-6606 [Electronic] United States
PMID	20147633 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S.)
Chemical References	Inflammation Mediators STAT6 Transcription Factor Stat6 protein, mouse Interleukin-4
Topics	Animals Cell Differentiation (genetics, immunology) Dermatitis, Atopic (genetics, immunology, pathology) Epidermis (immunology, pathology) Female Gene Expression Regulation (immunology) Genetic Predisposition to Disease Homeostasis (genetics, immunology) Humans Immunity, Innate (genetics) Inflammation Mediators (physiology) Interleukin-4 (deficiency, genetics, physiology) Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Permeability STAT6 Transcription Factor (biosynthesis, genetics, physiology) Up-Regulation (genetics, immunology)

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