Genetically defined variants of toll-like receptors 3, 7 and 9 as phenotype and risk modifier factors for psoriasis

In psoriasis, a chronic inflammatory skin disease with a complex pathophysiology, multiple epidermal differentiation and immune-related genes interact with environmental factors [1]. Despite recent findings on pathogenic related-immune cellular subsets and cytokines (e.g. Th17 and Th22 pathways), the ultimate factors that trigger and preserve inflammation remain unknown. TLRs are germ line-encoded pattern-recognition receptors that recognize pathogen-associated and molecular patterns (PAMPs) and tissue damage-associated molecular patterns (DAMPs) such as self-nucleic acids.