Skin Barrier Defects in Atopic Dermatitis

被引:153
作者
Agrawal, Rachana [1 ]
Woodfolk, Judith A. [1 ]
机构
[1] Univ Virginia Hlth Syst, Dept Med, Div Allergy, Charlottesville, VA 22908 USA
关键词
Atopic dermatitis; Th2; Inflammation; Skin barrier; Skin barrier defects; Tight junctions; Filaggrin; Defensins; Proteases; Ceramides; Epidermis; OF-FUNCTION MUTATIONS; SINGLE NUCLEOTIDE POLYMORPHISMS; THYMIC STROMAL LYMPHOPOIETIN; DOWN-REGULATES FILAGGRIN; INNATE IMMUNE-RESPONSE; STRATUM-CORNEUM; ANTIMICROBIAL PEPTIDES; ICHTHYOSIS VULGARIS; ENHANCED EXPRESSION; TH2; CYTOKINES;
D O I
10.1007/s11882-014-0433-9
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Atopic dermatitis (AD) is a chronic inflammatory skin condition with complex etiology that is dependent upon interactions between the host and the environment. Acute skin lesions exhibit the features of a Th2-driven inflammatory disorder, and many patients are highly atopic. The skin barrier plays key roles in immune surveillance and homeostasis, and in preventing penetration of microbial products and allergens. Defects that compromise the structural integrity or else the immune function of the skin barrier play a pivotal role in the pathogenesis of AD. This article provides an overview of the array of molecular building blocks that are essential to maintaining healthy skin. The basis for structural defects in the skin is discussed in relation to AD, with an emphasis on filaggrin and its genetic underpinnings. Aspects of innate immunity, including the role of antimicrobial peptides and proteases, are also discussed.
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页数:11
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