| First Author | McGee HM | Year | 2013 |
| Journal | J Invest Dermatol | Volume | 133 |
| Issue | 5 | Pages | 1321-9 |
| PubMed ID | 23223145 | Mgi Jnum | J:197959 |
| Mgi Id | MGI:5494940 | Doi | 10.1038/jid.2012.463 |
| Citation | McGee HM, et al. (2013) IL-22 promotes fibroblast-mediated wound repair in the skin. J Invest Dermatol 133(5):1321-9 |
| abstractText | Skin wound repair requires complex and highly coordinated interactions between keratinocytes, fibroblasts, and immune cells to restore the epidermal barrier and tissue architecture after acute injury. The cytokine IL-22 mediates unidirectional signaling from immune cells to epithelial cells during injury of peripheral tissues such as the liver and colon, where IL-22 causes epithelial cells to produce antibacterial proteins, express mucins, and enhance epithelial regeneration. In this study, we used IL-22(-/-) mice to investigate the in vivo role for IL-22 in acute skin wounding. We found that IL-22(-/-) mice displayed major defects in the skin's dermal compartment after full-thickness wounding. We also found that IL-22 signaling is active in fibroblasts, using in vitro assays with primary fibroblasts, and that IL-22 directs extracellular matrix (ECM) gene expression and myofibroblast differentiation both in vitro and in vivo. These data define roles of IL-22 beyond epithelial cross talk, and suggest that IL-22 has a previously unidentified role in skin repair by mediating interactions between immune cells and fibroblasts. |
