Abstract 152

The document presents the findings of a study on the role of TLR3, an innate immune receptor, in wound-induced hair neogenesis (WIHN) in mice. The study found that TLR3 is activated by molecules released during tissue damage and promotes the activation of developmental pathways for skin regeneration. Mice with a high regenerative capacity showed increased levels of TLR3 mRNA, and TLR3 knockout mice had greatly reduced regeneration. The addition of a TLR3 agonist increased hair regeneration, while inhibition of dsRNA decreased it. The effects of TLR3 on hair regeneration were dependent on IL6 and STAT3. In vitro, TLR3 activation prevented keratinocyte differentiation and upregulated stem cell genes. The study concludes that TLR3 activation may lead to improved cutaneous wound healing and hair follicle regeneration, representing a potential target for therapies aimed at enhancing adult regeneration and organogenesis in mammals.