UVB radiation illuminates the role of TLR3 in the epidermis.
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.
Division of Dermatology, Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Andrew W
AW
Borkowski
Division of Dermatology, Department of Medicine, University of California, San Diego, La Jolla, California, USA. Electronic address: RGallo@UCSD.edu.
Richard L
RL
Gallo
D004249:DNA Damage; D004817:Epidermis / Q000473:pathology* / Q000528:radiation effects*; D006801:Humans; D012871:Skin Diseases / Q000235:genetics* / Q000473:pathology*; D051196:Toll-Like Receptor 3 / Q000235:genetics*; D014466:Ultraviolet Rays / Q000009:adverse effects*
C495344:TLR3 protein, human; D051196:Toll-Like Receptor 3