Psoriasis is an inflammatory skin disease with a background of polygenic inheritance. Both environmental and genetic factors are involved in the etiology of the disease. In the last two decades, numerous studies have been conducted through linkage analysis, genome-wide association study (GWAS), and direct sequencing to explore the role of genetic variation in disease pathogenesis and progression. To date, >80 psoriasis susceptibility genes have been identified, including HLA-Cw6, IL12B, IL23R, and LCE3B/3C. Some genetic markers have been applied in disease prediction, clinical diagnosis, treatment, and new drug development, which could further explain the pathogenesis of psoriasis and promote the development of precision medicine. This review summarizes related research on genetic variation in psoriasis and explores implications of the findings in clinical application and the promotion of a personalized medicine project.
Many common diseases are characterized by polygenic architectures in which a single variant has only a small effect on phenotype. Genome-wide association studies and next generation sequencing have identified thousands of genetic variants of disease susceptibility. Recently, non-coding variants identified by genome-wide association studies have been systematically reviewed. Here, we review disease-causing coding variants and their relevance to clinical medicine.
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