Defects of corneocyte structural proteins and epidermal barrier in atopic dermatitis

被引:26
|
作者
Le Lamer, Marina [4 ]
Pellerin, Laurence [4 ]
Reynier, Marie [4 ]
Cau, Laura [4 ]
Pendaries, Valerie [4 ]
Leprince, Corinne [4 ]
Mechin, Marie-Claire [4 ]
Serre, Guy [4 ]
Paul, Carle [4 ,5 ]
Simon, Michel [1 ,2 ,3 ]
机构
[1] CHU Purpan, CNRS, UDEAR, UMR5165, F-31059 Toulouse 9, France
[2] Univ Toulouse, Toulouse, France
[3] Fac Med Toulouse, INSERM, U1056, F-31073 Toulouse, France
[4] Univ Toulouse 3, CNRS, INSERM, F-31062 Toulouse, France
[5] Toulouse Univ Hosp, Dept Dermatol, Toulouse, France
关键词
atopic dermatitis; corneocytes; eczema; epidermal barrier; filaggrin; keratinocytes; skin inflammation; FILAGGRIN NULL MUTATIONS; OF-FUNCTION MUTATIONS; PROTEASE BLEOMYCIN HYDROLASE; STRATUM-CORNEUM LIPIDS; ALLERGY CLIN IMMUNOL; SKIN BARRIER; STAPHYLOCOCCUS-AUREUS; TH2; CYTOKINES; FUNCTION VARIANTS; CHILDHOOD ECZEMA;
D O I
10.1515/hsz-2015-0141
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The main function of the epidermis is to establish a vital multifunctional barrier between the body and its external environment. A defective epidermal barrier is one of the key features of atopic dermatitis (AD), a chronic and relapsing inflammatory skin disorder that affects up to 20% of children and 2-3% of adults and often precedes the development of allergic rhinitis and asthma. This review summarizes recent discoveries on the origin of the skin barrier alterations in AD at the structural protein level, including hereditary and acquired components. The consequences of the epidermal barrier alteration on our current understanding of the pathogenesis of AD, and its possible implications on the treatment of patients, are discussed here.
引用
收藏
页码:1163 / 1179
页数:17
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