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Toll-like receptor 3 activation is required for normal skin barrier repair following UV damage.

  • Author(s): Borkowski, Andrew W
  • Kuo, I-Hsin
  • Bernard, Jamie J
  • Yoshida, Takeshi
  • Williams, Michael R
  • Hung, Nai-Jung
  • Yu, Benjamin D
  • Beck, Lisa A
  • Gallo, Richard L
  • et al.
Abstract

UV damage to the skin leads to the release of noncoding RNA (ncRNA) from necrotic keratinocytes that activates Toll-like receptor 3 (TLR3). This release of ncRNA triggers inflammation in the skin following UV damage. Recently, TLR3 activation was also shown to aid wound repair and increase the expression of genes associated with permeability barrier repair. Here, we sought to test whether skin barrier repair after UVB damage is dependent on the activation of TLR3. We observed that multiple ncRNAs induced expression of skin barrier repair genes, that the TLR3 ligand Poly (I:C) also induced expression and function of tight junctions, and that the ncRNA U1 acts in a TLR3-dependent manner to induce expression of skin barrier repair genes. These observations were shown to have functional relevance as Tlr3-/- mice displayed a delay in skin barrier repair following UVB damage. Combined, these data further validate the conclusion that recognition of endogenous RNA by TLR3 is an important step in the program of skin barrier repair.

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