Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.

2 型炎症是特应性皮炎皮肤屏障功能障碍的原因。

• 发表时间: Sep 2022
• 来源期刊: JID Innov
• DOI: 10.1016/j.xjidi.2022.100131
• PMID: 36059592
• 文章类型: Journal Article
• 作者列表: Beck LA,Cork MJ,Amagai M,De Benedetto A,Kabashima K,Hamilton JD,Rossi AB

关键词: AD, atopic dermatitis; AMP, antimicrobial peptide; CLDN, claudin; FFA, free fatty acid; ILC2, type 2 innate lymphoid cell; Jaki, Jak inhibitor; K, keratin; KC, keratinocyte; MMP, matrix metalloproteinase; NMF, natural moisturizing factor; PAR, protease-activated receptor; PDE-4, phosphodiesterase-4; SC, stratum corneum; SG, stratum granulosum; TCI, topical calcineurin inhibitor; TCS, topical corticosteroid; TEWL, transepidermal water loss; TJ, tight junction; TLR, toll-like receptor; TNF-α, tumor necrosis factor alpha; TYK, tyrosine kinase; Th, T helper; ZO, zona occludens; hBD, human β-defensin

Abstract

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.

摘要

皮肤屏障功能障碍,特应性皮炎（AD）的定义特征，来自多个相互作用的系统。在AD中,皮肤炎症是由宿主-环境相互作用引起的，涉及角质形成细胞以及组织驻留的免疫细胞，如2型先天淋巴细胞，嗜碱性粒细胞,肥大细胞,和2型辅助性T细胞，产生2型细胞因子，包括IL-4、IL-5、IL-13和IL-31。2型炎症广泛影响屏障功能相关基因的表达，如细胞内结构蛋白，细胞外脂，和连接蛋白，并增强金黄色葡萄球菌的皮肤定植。全身性抗2型炎症疗法可能会改善AD患者功能失调的皮肤屏障。