Abstract
Psoriasis is a chronic inflammatory dermatosis that contributes to approximately 1-5% of all skin disorders in Saudi Arabia. The genetic basis of psoriasis is supported by family based investigations; population based epidemiological studies, association studies with human leucocyte antigens (HLAs), genome-wide linkage scans, and candidate gene studies within and outside the major histocompatibility complex. Psoriasis represents a complex disease at the cellular, genomic and genetic levels, with infiltration of many types of leukocytes into the skin, altered growth and differentiation of skin-resident cells, and altered expression of more than 1,300 genes in psoriatic lesions. It is also apparent that there is considerable overlap between the molecular pathways that are involved in psoriasis and those that lead to other inflammatory or autoimmune diseases in humans. In this Review article, we describe the immune-genetic basis of psoriasis, the molecular pathways of pathogenic inflammation and the potential role of the genes that confer increased susceptibility to psoriasis.