| First Author | Sehra S | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 6 | Pages | 3186-90 |
| PubMed ID | 20147633 | Mgi Jnum | J:160119 |
| Mgi Id | MGI:4453436 | Doi | 10.4049/jimmunol.0901860 |
| Citation | Sehra S, et al. (2010) IL-4 regulates skin homeostasis and the predisposition toward allergic skin inflammation. J Immunol 184(6):3186-90 |
| abstractText | 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. |
