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| Update of genome-wide association study in atopic dermatitis |
| Li Meng, Yi-Chen Tang, Lian-Juan Yang* |
| Department of Dermatology, Shanghai Skin Disease Hospital, Shanghai 200443, China. |
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Abstract Atopic dermatitis is a common inflammatory disease caused by multiple factors including genetic predisposition, immune dysregulation, and external environmental factors. Genome-wide association study is a relatively comprehensive and unbiased approach to identify the genetic components of polygenic inheritance diseases and is helpful to discover the cellular pathways underlying them. To date, a total of 33 associated loci with a genome-wide level of significance (P < 5x10-8) have been identified in atopic dermatitis by genome-wide association studies, Meta-analysis of genome-wide association studies and immuno-chip analysis study. Atopic dermatitis is often accompanied by asthma，allergic rhinitis or hay fever. Genome-wide association studies have identified nearly 100 common genetic susceptibility loci for atopic dermatitis and these allergic diseases, which indicated that atopic dermatitis and these allergic diseases partly coexist might because they share many?genetic risk variants which dysregulate?the??of?immune-related?genes. In addition, 12 new loci of atopic dermatitis were identified by research based on existing genome-wide association data. All these associated loci have implied a large number of susceptibility genes of atopic dermatitis. However, little is known about their function in atopic dermatitis development except the FLG gene, which is most strongly associated with atopic dermatitis. But not all individuals with FLG variants occur atopic dermatitis. Genome-wide association studies have improved our understanding of disease mechanisms of atopic dermatitis and will generate potential therapeutic opportunities. However, further replication, fine mapping and functional studies are needed.
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Received: 14 October 2016
Published: 15 January 2019
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Corresponding Authors:
Dr. Lian-Juan Yang
E-mail: drrichard01@126.com
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2018, Vol. 1 
