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The interplay between genetic and environmental factors in the pathogenesis of atopic dermatitis
Author(s) -
Otsuka Atsushi,
Nomura Takashi,
Rerknimitr Pawinee,
Seidel Judith A.,
Honda Tetsuya,
Kabashima Kenji
Publication year - 2017
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12545
Subject(s) - filaggrin , atopic dermatitis , immunology , pathogenesis , dupilumab , disease , allergy , etiology , medicine , genetic predisposition , inflammation , mechanism (biology) , dermatology , biology , pathology , philosophy , epistemology
Summary 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 α 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.