期刊
CLINICAL COSMETIC AND INVESTIGATIONAL DERMATOLOGY
卷 15, 期 -, 页码 2621-2628出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/CCID.S391360
关键词
intrinsic atopic dermatitis; extrinsic atopic dermatitis; epidermal barrier; immune dysfunction; immune globulin E
类别
资金
- National Natural Science Foundation of China
- [82073442]
- [82273529]
Recent research in atopic dermatitis (AD) has revealed a complex disease profile with different subtypes and underlying molecular mechanisms. One of the most common classifications is based on extrinsic and intrinsic factors, which are determined by serum IgE levels and/or specific IgE responses to allergens. Extrinsic AD is the most common type, characterized by high IgE, impaired skin barrier, and comorbid atopic diseases. Intrinsic AD, accounting for 20% of AD cases, has normal IgE levels and intact barrier function. Clinical studies have shown that extrinsic AD is a classic Th2-based inflammatory dermatitis, while the intrinsic subtype presents increased Th1/Th17/Th22 cytokines but normal Th2 cytokines.
In atopic dermatitis (AD), recent research advances have portrayed a complex disease profile based on different subtypes/ phenotypes and underlying molecular mechanisms/endotypes. Extrinsic and intrinsic subdivision is one of the most common types, defined in terms of total serum immune globulin E (IgE) and/or specific IgE to food and environmental allergens. Extrinsic AD is the most common type (80%), with high IgE, impaired skin barrier, as well as high incidence of comorbid atopic diseases, whereas intrinsic AD accounted for 20% of AD, with normal IgE and intact barrier function. Clinical studies have shown that extrinsic AD was a classic Th2-based inflammatory dermatitis, while the intrinsic subtype presented increased Th1/Th17/Th22 but normal Th2 cytokines. Protein sensitization, a classic Th2 response, has been clearly characterized in extrinsic AD, while metal hapten induces intrinsic AD's sensitization, which may be associated with suprabasin deficiency. In this review, we aimed to further expand our knowledge about similarities and differences between these two subtypes, which will expand our capability to further dissect pathophysiology of AD and enable us to develop personalized medicine approaches.
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