UVB-Induced Skin Inflammation and Cutaneous Tissue Injury Is Dependent on the MHC Class I-Like Protein, CD1d.

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Serval ID
serval:BIB_E4DC7A90FAB2
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
UVB-Induced Skin Inflammation and Cutaneous Tissue Injury Is Dependent on the MHC Class I-Like Protein, CD1d.
Journal
Journal of Investigative Dermatology
Author(s)
Ryser S., Schuppli M., Gauthier B., Hernandez D.R., Roye O., Hohl D., German B., Holzwarth J.A., Moodycliffe A.M.
ISSN
1523-1747 (Electronic)
ISSN-L
0022-202X
Publication state
Published
Issued date
2014
Volume
134
Number
1
Pages
192-202
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
CD1d is a major histocompatibility complex class 1-like molecule that regulates the function and development of natural killer T (NKT) cells. Previously, we identified a critical role for the CD1d-NKT cell arm of innate immunity in promoting the development of UVB-induced p53 mutations, immune suppression, and skin tumors. Sunburn, an acute inflammatory response to UVB-induced cutaneous tissue injury, represents a clinical marker for non-melanoma skin cancer (NMSC) risk. However, the innate immune mechanisms controlling sunburn development are not considered relevant in NMSC etiology, and remain poorly investigated. Here we found that CD1d knockout (CD1d(-/-)) mice resist UVB-induced cutaneous tissue injury and inflammation compared with wild-type (WT) mice. This resistance was coupled with a faster epithelial tissue healing response. In contrast, the skins of UVB-irradiated invariant NKT cell-knockout (Jα18(-/-)) and NKT cell-deficient (TCRα(-/-)) mice, which express CD1d but are deficient in CD1d-dependent NKT cells, exhibited as much cutaneous tissue injury and inflammation as WT mice. In the absence of NKT cells, CD1d-deficient keratinocytes, dendritic cells, and macrophages exhibited diminished basal and stress-induced levels of pro-inflammatory mediators. Thus, our findings identify an essential role for CD1d in promoting UVB-induced cutaneous tissue injury and inflammation. They also suggest sunburn and NMSC etiologies are immunologically linked.
Pubmed
Web of science
Open Access
Yes
Create date
16/01/2014 16:40
Last modification date
20/08/2019 16:08
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