期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 6, 页码 3186-3190出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0901860
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资金
- National Institutes of Health [U19A1070448, RO1AR41256]
- Veteran's Administration Merit Award
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. The Journal of Immunology, 2010, 184: 3186-3190.
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