The Pattern Recognition Receptor Toll-Like Receptor 3 Regulates Skin Barrier Homeostasis
January 2014
in “
eScholarship (California Digital Library)
”
Toll-like receptor 3 TLR3 skin barrier repair UV damage non-coding double-stranded RNA dsRNA keratinocytes ABCA12 glucocerebrosidase tight junction function lipid production Tlr3-/- mice UVB damage scavenger receptors Msr1-/- mice IL-1R signaling Il1r-/- mice dermal hair cysts macrophages skin barrier UV exposure RNA skin cells lipids immune response
TLDR Toll-like receptor 3 helps repair the skin barrier after UV damage.
The study explored the role of Toll-like receptor 3 (TLR3) in skin barrier repair following UV damage. It was found that non-coding double-stranded RNA (dsRNA) from damaged keratinocytes activated TLR3, leading to increased expression of genes involved in skin barrier repair, such as ABCA12 and glucocerebrosidase. TLR3 activation also enhanced tight junction function and lipid production in keratinocytes. Tlr3-/- mice showed delayed skin barrier repair after UVB damage, highlighting TLR3's role in this process. Additionally, scavenger receptors were found to facilitate dsRNA entry into keratinocytes, influencing gene expression related to barrier repair. Msr1-/- mice exhibited defects in skin barrier repair, indicating the importance of scavenger receptors. The study also revealed that IL-1R signaling is crucial for skin homeostasis post-UVB exposure, as Il1r-/- mice developed dermal hair cysts and had fewer macrophages. Overall, the research provided insights into the cellular mechanisms involved in skin response to UVB damage.