Psoriasis is a chronic inflammatory disease of the skin. The causes of psoriasis are unknown, although family and twin studies have shown genetic factors to play a key role in its development. The many genes associated with psoriasis and the immune response include TNFα, IL23, and IL12. Advances in knowledge of the pathogenesis of psoriasis have enabled the development of new drugs that target cytokines (e.g., etanercept, adalimumab, and infliximab, which target TNFα, and ustekinumab, which targets the p40 subunit of IL23 and IL12). These drugs have improved the safety and efficacy of treatment in comparison with previous therapies. However, not all patients respond equally to treatment, possibly owing to interindividual genetic variability. In this review, we describe the genes associated with psoriasis and the immune response, the biological drugs used to treat chronic severe plaque psoriasis, new drugs in phase II and III trials, and current knowledge on the implications of pharmacogenomics in predicting response to these treatments. 1. Introduction Psoriasis is a chronic inflammatory disease of the skin which is characterized by the presence of erythematous scaly plaques [1]. The prevalence of psoriasis is 2-3% worldwide [2]. Psoriasis has a negative impact on the patient’s health and quality of life, is associated with serious medical comorbidities, and affects the quality of life of family members [3, 4]. While the exact cause of psoriasis is unknown, genetic and environmental factors play an important role in its development [5]. The environmental factors that appear to influence the course of and the susceptibility to psoriasis include chronic infections, stress, low humidity, drugs (beta-blockers, lithium, antimalarial agents, and interferon), smoking, and obesity [6]. The role of genetics in the pathogenesis of the disease is well documented in family and twin studies [7]. Genetic factors have been well studied in candidate-driven gene-specific studies and in genomewide association studies (GWAS). The genome regions most strongly associated with the development of the disease are associated with the immune system. Interleukin 23 receptor (IL23R), IL12B, and the human leukocyte antigen Cw6 (HLA-Cw6) of the major histocompatibility complex have been strongly associated with psoriasis [8]. Several studies have described the important role of single-nucleotide polymorphisms (SNPs) in the promoter region of the tumour necrosis factor gene (TNFα) [8]. Discovery of such consistent associations has enabled the development of new, more effective drugs
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