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Critical Reviews™ in Immunology
インパクトファクター: 1.352 5年インパクトファクター: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN 印刷: 1040-8401
ISSN オンライン: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v28.i1.20
pages 15-43

Scratching the Surface: Towards Understanding the Pathogenesis of Atopic Dermatitis

Sarita Sehra
Departments of Pediatrics and HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202
Florencia M. Barbe Tuana
Departments of Pediatrics and HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202
Mark Holbreich
Departments of Dermatology, Indiana University School of Medicine, Indianapolis, IN 46202
Nico Mousdicas
Departments of Dermatology, Indiana University School of Medicine, Indianapolis, IN 46202
Robert S. Tepper
Departments of Pediatrics and HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202
Cheong-Hee Chang
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109
Jeffrey B. Travers
Departments of Dermatology, and HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202
Mark H. Kaplan
Departments of Pediatrics and HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202

要約

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a steadily increasing prevalence affecting 10%−20% of infants and 1%−3% of adults globally. It is often the first clinical manifestation of atopic disease preceding asthma and allergic rhinitis. At least half of the children with AD develop some other form of atopic disease later in life. The pathogenesis of AD involves a complex interplay of factors, including genetic predisposition due to altered immune or skin barrier function, interactions with the environment, and infectious triggers of inflammation. In this review, we summarize the recent advances in understanding the contribution of different factors in the pathophysiology of AD in human and animal model systems. These insights provide new therapeutic potential for the treatment of human AD.


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