The interplay between genetic and environmental factors in the pathogenesis of atopic dermatitis

被引：146

作者：

Otsuka, Atsushi ^{[1
]}

Nomura, Takashi ^{[1
]}

Rerknimitr, Pawinee ^{[1
,2
]}

Seidel, Judith A. ^{[1
]}

Honda, Tetsuya ^{[1
]}

Kabashima, Kenji ^{[1
,3
,4
]}

机构：

[1] Kyoto Univ, Grad Sch Med, Dept Dermatol, Kyoto, Japan

[2] Chulalongkorn Univ, Fac Med, Allergy & Clin Immunol Res Grp, Div Dermatol,Dept Med, Bangkok, Thailand

[3] ASTAR, Singapore Immunol Network SIgN, Biopolis, Singapore, Singapore

[4] ASTAR, Inst Med Biol, Biopolis, Singapore, Singapore

来源：

IMMUNOLOGICAL REVIEWS | 2017年 / 278卷 / 01期

关键词：

allergy; inflammation; skin; INNATE LYMPHOID-CELLS; THYMIC STROMAL LYMPHOPOIETIN; REGULATORY T-CELLS; CYCLIC-AMP-PHOSPHODIESTERASE; ANTIGEN-PRESENTING CELLS; ANTI-CD20 RITUXIMAB TREATMENT; NATURAL HELPER-CELLS; CLASS-II COMPLEXES; FLAKY TAIL MICE; DENDRITIC CELLS;

D O I：

10.1111/imr.12545

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Atopic dermatitis (AD) is a chronic skin disorder characterized by pruritus and recurrent eczematous lesions that are accompanied by T-helper (Th)2-dominated inflammation. AD Etiology is not yet completely understood, but it is multifactorial. Moreover, the disease is characterized by complex interactions between genetic and environmental factors, such as skin barrier dysfunctions, allergy/immunity, and pruritus. For example, filaggrin is a key protein involved in skin barrier function. Th2 cells produce interleukin (IL)-31, which provokes pruritus, and other Th2 cytokines decrease filaggrin expression by keratinocytes. Dupilumab has recently been developed for AD treatment; its mechanism of action is to bind to IL-4 receptor alpha and inhibit downstream signaling induced by IL-4 and IL-13. This review summarizes the etiopathogenesis of AD and provides the rationale for selecting a novel targeted therapy.

引用

页码：246 / 262

页数：17

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