TLR3 and inflammatory skin diseases: From environmental factors to molecular opportunities

Abstract

Toll-like receptors (TLRs) are cellular sensors designed to recognize pathogens. TLR3 recognizes viral double-stranded RNA, which is a molecular pattern produced by most viruses. Interestingly, there is increasing recognition of the role of TLR3 in non-infectious inflammatory diseases as well as viral infections. In addition, TLR3 recognizes not only exogenous threats such as virus but also endogenous host molecules associated with tissue injury. TLR3 is expressed on various cell types including keratinocytes, Langerhans cells, mast cells, and fibroblasts in the skin. Recent findings show that upon stimulation of TLR3 with exogenous or endogenous ligands, these cells are closely involved in the pathogenesis of infectious or inflammatory skin diseases such as viral infections or allergic and irritant contact dermatitis. Furthermore, TLR3 signaling is associated with barrier repair Skin barrier repair after tissue injury and itching sensation in the skin. Therefore, TLR3 may serve as a new therapeutic target for inflammatory skin diseases.