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Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis

2022; Elsevier BV; Volume: 2; Issue: 5 Linguagem: Inglês

10.1016/j.xjidi.2022.100131

2667-0267

Lisa A. Beck, Michael J. Cork, Masayuki Amagai, Anna De Benedetto, Kenji Kabashima, Jennifer D. Hamilton, Ana B. Rossi,

Exercise and Physiological Responses

Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host-environment interactions involving keratinocytes as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T helper type 2 cells, which produce type 2 cytokines, including IL-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts the expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances Staphylococcus aureus skin colonization. Systemic anti‒type 2 inflammation therapies may improve dysfunctional skin barrier in AD.