%0 Journal Article
%T Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.
%A Beck LA
%A Cork MJ
%A Amagai M
%A De Benedetto A
%A Kabashima K
%A Hamilton JD
%A Rossi AB
%J JID Innov
%V 2
%N 5
%D Sep 2022
%M 36059592
暂无%R 10.1016/j.xjidi.2022.100131
%X 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.