| First Author | Sivaprasad U | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 11 | Pages | 6802-8 |
| PubMed ID | 20971924 | Mgi Jnum | J:167566 |
| Mgi Id | MGI:4868549 | Doi | 10.4049/jimmunol.1002118 |
| Citation | Sivaprasad U, et al. (2010) IL-13Ralpha2 has a protective role in a mouse model of cutaneous inflammation. J Immunol 185(11):6802-8 |
| abstractText | IL-13 is expressed in lesions of atopic dermatitis (AD) and has been associated with increased disease severity. IL-13 has two cognate receptors: IL-13Ralpha1 and IL-13Ralpha2. Although IL-13Ralpha2 expression is known to be induced in response to IL-13 in keratinocytes, its function in AD has never been evaluated. We characterized the loss of skin barrier function and the development of cutaneous inflammation in IL-13Ralpha2-null versus wild-type BALB/c mice following an epicutaneous allergen-sensitization/challenge model that shares similarities with human AD. Mice lacking IL-13Ralpha2 had significantly increased transepidermal water loss, cutaneous inflammation, peripheral eosinophilia, and IgG1 and IgE levels compared with wild-type mice. The rate of resolution of the cutaneous inflammation was not significantly altered in the IL-13Ralpha2-null mice. IL-13 induced expression of IL-13Ralpha2 in keratinocyte cell lines and primary human keratinocytes. Depletion of IL-13Ralpha2 in a keratinocyte cell line resulted in increased STAT6 signaling in response to IL-13. In conclusion, IL-13Ralpha2 serves a protective role in the pathogenesis of allergic inflammation and loss of skin barrier function in a mouse model of AD, suggesting that it may be an important endogenous regulator of IL-13-induced cutaneous inflammation in humans. |
