UVB Radiation Illuminates the Role of TLR3 in the Epidermis

被引：20

作者：

Borkowski, Andrew W. ^{[1
]}

Gallo, Richard L. ^{[1
]}

机构：

[1] Univ Calif San Diego, Div Dermatol, Dept Med, La Jolla, CA 92093 USA

来源：

JOURNAL OF INVESTIGATIVE DERMATOLOGY | 2014年 / 134卷 / 09期

关键词：

TOLL-LIKE RECEPTOR-3; DOUBLE-STRANDED-RNA; CELL-DEATH; DYING CELLS; PROGRAMMED NECROSIS; HMGB1; RELEASE; DANGER SIGNAL; IMMUNE-SYSTEM; ULTRAVIOLET-B; SKIN;

D O I：

10.1038/jid.2014.167

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

UV radiation poses a significant risk to human health. The mechanisms that help repair UV-damaged cells have recently been more clearly defined with the observation that Toll-like receptor 3 can sense self RNA released from necrotic keratinocytes following UV damage. TLR3 activation in the skin induces inflammation and increases the expression of genes involved in skin barrier repair. Activation of TLR2 in the skin by commensal microbial products prevents excessive inflammation by blocking downstream TLR3 signaling. This review highlights how UV damage induced inflammation in the skin is propagated by host products and regulated by host inhabitants.

引用

页码：2315 / 2320

页数：6

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