IL-27 Facilitates Skin Wound Healing through Induction of Epidermal Proliferation and Host Defense.
Conference Paper
Skin wound repair requires a coordinated program of epithelial cell proliferation and differentiation as well as resistance to invading microbes. However, the factors that trigger epithelial cell proliferation in this inflammatory process are incompletely understood. In this study, we demonstrate that IL-27 is rapidly and transiently produced by CD301b+ cells in the skin after injury. The functional role of IL-27 and CD301b+ cells is demonstrated by the finding that CD301b-depleted mice exhibit delayed wound closure in vivo, which could be rescued by topical IL-27 treatment. Furthermore, genetic ablation of the IL-27 receptor (Il27Ra-/-) attenuates wound healing, suggesting an essential role for IL-27 signaling in skin regeneration in vivo. Mechanistically, IL-27 feeds back on keratinocytes to stimulate cell proliferation and re-epithelialization in the skin, whereas IL-27 leads to suppression of keratinocyte terminal differentiation. Finally, we identify that IL-27 potently increases expression of the antiviral oligoadenylate synthetase 2, but does not affect expression of antibacterial human beta defensin 2 or regenerating islet-derived protein 3-alpha. Together, our data suggest a previously unrecognized role for IL-27 in regulating epithelial cell proliferation and antiviral host defense during the normal wound healing response.
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Duke Authors
Cited Authors
- Yang, B; Suwanpradid, J; Sanchez-Lagunes, R; Choi, HW; Hoang, P; Wang, D; Abraham, SN; MacLeod, AS
Published Date
- May 2017
Published In
Volume / Issue
- 137 / 5
Start / End Page
- 1166 - 1175
PubMed ID
- 28132857
Pubmed Central ID
- PMC5552041
Electronic International Standard Serial Number (EISSN)
- 1523-1747
Digital Object Identifier (DOI)
- 10.1016/j.jid.2017.01.010
Conference Location
- United States