期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 137, 期 11, 页码 2417-2426出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2017.07.814
关键词
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类别
资金
- National Institutes of Health [R01AR052728, R01AI052453, R01AR06781, R01 ES016629-01A1]
- UCSD Dermatologist Investigator Training Program [T32AR062496]
- National Cancer Institute of the National Institutes of Health [T32CA106195]
In this study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r(-/-)) or deficient in IL1-beta developed multiple epidermal cysts after chronic UVB exposure. Cysts that developed in IL1r(-/-) mice were characterized by the presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal melanocyte distribution and retinoid X receptor-alpha expression. The increased incidence of cysts in IL1r(-/-) mice was associated with less skin inflammation as characterized by decreased recruitment of macrophages, and their skin also maintained epidermal barrier function compared with wild-type mice. Transcriptional analysis of the skin of IL1r(-/-) mice after UVB exposure showed decreased gene expression of proinflammatory cytokines such as tumor necrosis factor-alpha and IL-6. In vitro, primary keratinocytes derived from IL1r(-/-) mice were more resistant to UVB-triggered cell death compared with wild-type cells, and tumor necrosis factor-alpha release was completely blocked in the absence of IL-1R. These observations illustrate an unexpected yet prominent phenotype associated with the lack of IL-1R signaling in mice and support further investigation into the role of IL-1 ligands in epidermal repair and innate immune response after damaging UVB exposure.
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