Genetic Epidemiology of Psoriasis

被引:143
作者
Gupta R. [1 ]
Debbaneh M.G. [1 ,2 ]
Liao W. [1 ]
机构
[1] Department of Dermatology, University of California, San Francisco, San Francisco, CA, 94143
[2] School of Medicine, University of California, Irvine, Irvine, CA
关键词
Epidemiology; Genetic; Pathogenesis; Prevalence; Psoriasis;
D O I
10.1007/s13671-013-0066-6
中图分类号
学科分类号
摘要
Psoriasis is a chronic, inflammatory, immune-mediated skin condition with a prevalence of 0-11.8 % across the world. It is associated with a number of cardiovascular, metabolic, and autoimmune disease comorbidities. Psoriasis is a multifactorial disorder, influenced by both genetic and environmental factors. Its genetic basis has long been established through twin studies and familial clustering. The association of psoriasis with the HLA-Cw6 allele has been shown in many studies. Recent genome-wide association studies have identified a large number of other genes associated with psoriasis. Many of these genes regulate the innate and adaptive immune system. These findings indicate that a dysregulated immune system may play a major role in the pathogenesis of psoriasis. In this article, we review the clinical and genetic epidemiology of psoriasis with a brief description of the pathogenesis of disease. © 2014 Springer Science+Business Media New York.
引用
收藏
页码:61 / 78
页数:17
相关论文
共 159 条
[1]
Koo J., Population-based epidemiologic study of psoriasis with emphasis on quality of life assessment, Dermatol Clin, 14, 3, pp. 485-496, (1996)
[2]
Nestle F.O., Kaplan D.H., Barker J., Psoriasis, N Engl J Med, 361, 5, pp. 496-509, (2009)
[3]
Stern R.S., Nijsten T., Feldman S.R., Margolis D.J., Rolstad T., Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction, J Investig Dermatol Symp Proc, 9, 2, pp. 136-139, (2004)
[4]
Chandran V., Raychaudhuri S.P., Geoepidemiology and environmental factors of psoriasis and psoriatic arthritis, J Autoimmun, 34, 3, (2010)
[5]
Christophers E., Psoriasis-epidemiology and clinical spectrum, Clin Exp Dermatol, 26, 4, pp. 314-320, (2001)
[6]
de Cid R., Riveira-Munoz E., Zeeuwen P.L., Robarge J., Liao W., Dannhauser E.N., Et al., Deletion of the late cornified envelope LCE3B and LCE3C genes as a susceptibility factor for psoriasis, Nat Genet, 41, 2, pp. 211-215, (2009)
[7]
Ellinghaus D., Ellinghaus E., Nair R.P., Stuart P.E., Esko T., Metspalu A., Et al., Combined analysis of genome-wide association studies for Crohn disease and psoriasis identifies seven shared susceptibility loci, Am J Human Genet, 90, 4, pp. 636-647, (2012)
[8]
Ellinghaus E., Ellinghaus D., Stuart P.E., Nair R.P., Debrus S., Raelson J.V., Et al., Genome-wide association study identifies a psoriasis susceptibility locus at TRAF3IP2, Nat Genet, 42, 11, pp. 991-995, (2010)
[9]
Nair R.P., Duffin K.C., Helms C., Ding J., Stuart P.E., Goldgar D., Et al., Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways, Nat Genet, 41, 2, pp. 199-204, (2009)
[10]
Strange A., Capon F., Spencer C.C., Knight J., Et al., A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1, Nat Genet, 42, 11, pp. 985-990, (2010)