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Targeting Skin Barrier Function in Atopic Dermatitis

皮肤屏障 特应性皮炎 皮肤病科 医学
作者
Ellen H. van den Bogaard,Peter M. Elias,Elena Goleva,Evgeny Berdyshev,Jos P.H. Smits,Simon G. Danby,Michael J. Cork,Donald Y.M. Leung
出处
期刊:The Journal of Allergy and Clinical Immunology: In Practice [Elsevier]
卷期号:11 (5): 1335-1346 被引量:55
标识
DOI:10.1016/j.jaip.2023.02.005
摘要

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease in the general population. Skin barrier dysfunction is the central abnormality leading to AD. The cause of skin barrier dysfunction is complex and rooted in genetic mutations, interactions between the immune pathway activation and epithelial cells, altered host defense mechanisms, as well as environmental influences that cause epithelial cell activation and release of alarmins (such as thymic stromal lymphopoietin) that can activate the type 2 immune pathway, including generation of interleukins 4 and 13, which induces defects in the skin barrier and increased allergic inflammation. These inflammatory pathways are further influenced by environmental factors including the microbiome (especially Staphylococcus aureus), air pollution, stress, and other factors. As such, AD is a syndrome involving multiple phenotypes, all of which have in common skin barrier dysfunction as a key contributing factor. Understanding mechanisms leading to skin barrier dysfunction in AD is pointing to the development of new topical and systemic treatments in AD that helps keep skin borders secure and effectively treat the disease. Atopic dermatitis (AD) is the most common chronic inflammatory skin disease in the general population. Skin barrier dysfunction is the central abnormality leading to AD. The cause of skin barrier dysfunction is complex and rooted in genetic mutations, interactions between the immune pathway activation and epithelial cells, altered host defense mechanisms, as well as environmental influences that cause epithelial cell activation and release of alarmins (such as thymic stromal lymphopoietin) that can activate the type 2 immune pathway, including generation of interleukins 4 and 13, which induces defects in the skin barrier and increased allergic inflammation. These inflammatory pathways are further influenced by environmental factors including the microbiome (especially Staphylococcus aureus), air pollution, stress, and other factors. As such, AD is a syndrome involving multiple phenotypes, all of which have in common skin barrier dysfunction as a key contributing factor. Understanding mechanisms leading to skin barrier dysfunction in AD is pointing to the development of new topical and systemic treatments in AD that helps keep skin borders secure and effectively treat the disease. Challenging Best Practice of Atopic DermatitisThe Journal of Allergy and Clinical Immunology: In PracticeVol. 11Issue 5PreviewThis issue of JACI: In Practice provides reviews of 3 important and topical aspects of atopic dermatitis (AD) management relating to (1) skin barrier function, (2) topical and systemic immune modulator therapies, and (3) the challenges of managing AD in the underprivileged and ethnic minorities. The objective is to present the latest evidence base to allow the reader to consolidate their best practice, as well as critically evaluate the pros and cons of commonly used and novel therapies for AD. Full-Text PDF
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