Psoriasis genetics: breaking the barrier

被引:190
|
作者
Roberson, Elisha D. O. [1 ]
Bowcock, Anne M. [1 ]
机构
[1] Washington Univ, Sch Med, Dept Genet, Div Human Genet, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
GENOME-WIDE ASSOCIATION; EPIDERMAL DIFFERENTIATION COMPLEX; NF-KAPPA-B; ATOPIC-DERMATITIS; T-CELL; TRANSGENIC MICE; RHEUMATOID-ARTHRITIS; DENDRITIC CELLS; SKIN-DISEASE; EXPRESSION;
D O I
10.1016/j.tig.2010.06.006
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Psoriasis is a common incurable inflammatory skin disease affecting 2-3% of the European population. Psoriatic skin contains large numbers of immune cells which produce many cytokines, chemokines and inflammatory molecules. The epidermis divides much faster than normal and has a defective outer layer or barrier which under normal circumstances protects from infection and dehydration. Psoriatic skin is characterized by a distinct set of inflammation and epidermal proliferation and differentiation markers, and it has been unclear whether the genetic basis of psoriasis reflects defects of the immune system or of the skin. One genetic determinant lies within the major histocompatibility complex class 1 region. Genome-wide association studies have revealed genetic susceptibility factors that play a role in the formation of immune cells found in psoriasis lesions. Others affect epidermal proliferation and skin barrier formation. Hence, genetic components of both the immune system and the epidermis can predispose to disease.
引用
收藏
页码:415 / 423
页数:9
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