Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases

被引：279

作者：

Kubo, Akiharu ^{[2
]}

Nagao, Keisuke

Amagai, Masayuki ^{[1
]}

机构：

[1] Keio Univ, Sch Med, Dept Dermatol, Shinjuku Ku, Tokyo 1608582, Japan

[2] Keio Univ, Sch Med, Ctr Integrated Med Res, Tokyo 1608582, Japan

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2012年 / 122卷 / 02期

关键词：

THYMIC STROMAL LYMPHOPOIETIN; PROTEASE BLEOMYCIN HYDROLASE; EPITHELIAL TIGHT JUNCTIONS; DOWN-REGULATES FILAGGRIN; OF-FUNCTION MUTATIONS; LANGERHANS CELLS; STRATUM-CORNEUM; DENDRITIC CELLS; NETHERTON-SYNDROME; CONTACT SENSITIZATION;

D O I：

10.1172/JCI57416

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Classic atopic dermatitis is complicated by asthma, allergic rhinitis, and food allergies, cumulatively referred to as atopic diseases. Recent discoveries of mutations in the filaggrin gene as predisposing factors for atopic diseases have refocused investigators' attention on epidermal barrier dysfunction as a causative mechanism. The skin's barrier function has three elements: the stratum corneum (air-liquid barrier), tight junctions (liquid-liquid barrier), and the Langerhans cell network (immunological barrier). Clarification of the molecular events underpinning epidermal barrier function and dysfunction should lead to a better understanding of the pathophysiological mechanisms of atopic diseases.

引用

页码：440 / 447

页数：8

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