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学科主题临床医学
Molecular Biology of Atopic Dermatitis
Mu, Zhanglei1; Zhao, Yan1; Liu, Xiaojing1; Chang, Christopher2; Zhang, Jianzhong1
关键词Molecular Biology Atopic Dermatitis Eczema Filaggrin Cathelicidin Atopy Atopic March Ige Thymic Stromal Lymphopoeitin Tumor Necrosis Factor-alpha
刊名CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
2014-10-01
DOI10.1007/s12016-014-8415-1
47期:2页:193-218
收录类别SCI
文章类型Review
WOS标题词Science & Technology
类目[WOS]Allergy ; Immunology
研究领域[WOS]Allergy ; Immunology
关键词[WOS]THYMIC STROMAL LYMPHOPOIETIN ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; GENOME-WIDE ASSOCIATION ; OF-FUNCTION MUTATIONS ; SKIN BARRIER FUNCTION ; EOSINOPHIL-DERIVED NEUROTOXIN ; SERUM IGE LEVELS ; TOLL-LIKE RECEPTOR-2 ; NF-KAPPA-B ; CD14 PROMOTER POLYMORPHISMS
英文摘要

Atopic dermatitis (AD) is a chronic inflammatory skin disease with specific genetic and immunological mechanisms. The rapid development of new techniques in molecular biology had ushered in new discoveries on the role of cytokines, chemokines, and immune cells in the pathogenesis of AD. New polymorphisms of AD are continually being reported in different populations. The physical and immunological barrier of normal intact skin is an important part of the innate immune system that protects the host against microbials and allergens that are associated with AD. Defects in the filaggrin gene FLG may play a role in facilitating exposure to allergens and microbial pathogens, which may induce Th2 polarization. Meanwhile, Th22 cells also play roles in skin barrier impairment through IL-22, and AD is often considered to be a Th2/Th22-dominant allergic disease. Mast cells and eosinophils are also involved in the inflammation via Th2 cytokines. Release of pruritogenic substances by mast cells induces scratching that further disrupts the skin barrier. Th1 and Th17 cells are mainly involved in chronic phase of AD. Keratinocytes also produce proinflammatory cytokines such as thymic stromal lymphopoietin (TSLP), which can further affect Th cells balance. The immunological characteristics of AD may differ for various endotypes and phenotypes. Due to the heterogeneity of the disease, and the redundancies of these mechanisms, our knowledge of the pathophysiology of the disease is still incomplete, which is reflected by the absence of a cure for the disease.

语种英语
WOS记录号WOS:000342145600008
引用统计
被引频次:20[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52523
专题北京大学第二临床医学院_皮科
作者单位1.Peking Univ Peoples Hosp, Dept Dermatol, Beijing 100044, Peoples R China
2.Thomas Jefferson Univ, Div Allergy & Immunol, Nemours AI duPont Hosp Children, Wilmington, DE 19803 USA
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GB/T 7714
Mu, Zhanglei,Zhao, Yan,Liu, Xiaojing,et al. Molecular Biology of Atopic Dermatitis[J]. CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY,2014,47(2):193-218.
APA Mu, Zhanglei,Zhao, Yan,Liu, Xiaojing,Chang, Christopher,&Zhang, Jianzhong.(2014).Molecular Biology of Atopic Dermatitis.CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY,47(2),193-218.
MLA Mu, Zhanglei,et al."Molecular Biology of Atopic Dermatitis".CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY 47.2(2014):193-218.
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