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

Sarita Sehra, Yongxue Yao, Michael D. Howell, Evelyn T. Nguyen, Geoffrey S. Kansas, Donald Y.M. Leung, Jeffrey B. Travers, Mark H. Kaplan

Research output: Contribution to journalArticle

102 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)3186-3190
Number of pages5
JournalJournal of Immunology
Issue number6
StatePublished - Mar 15 2010


ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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