Toll-like receptors (TLR) are cell membrane receptors at the interface of the innate and adaptative immunity. Located at the extracellular surface of keratinocytes, TLR recognizes conserved motifs from pathogens (microbial pathogen-associated molecular patterns, PAMPs) to activate inflammatory cellular pathways. TLR-induced cell signaling leads to the activation of nuclear factor-kappa B (NF-kB) and mitogen-activated protein kinases (MAPKs), subsequently inducing key inflammatory cytokines production.
Even though the activation of TLR belongs to the regular immune response, their over-activation has been related to various inflammatory diseases such as atopic dermatitis, psoriasis or acne. TLR-based treatments are therefore promising solutions to solve skin inflammatory diseases and infections.
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