Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis

被引：144

作者：

Beck, Lisa A. ^{[1
]}

Cork, Michael J. ^{[2
]}

Amagai, Masayuki ^{[3
,4
]}

De Benedetto, Anna ^{[1
]}

Kabashima, Kenji ^{[5
]}

Hamilton, Jennifer D. ^{[6
]}

Rossi, Ana B. ^{[7
]}

机构：

[1] Univ Rochester, Med Ctr, Dept Dermatol, 601 Elmwood Ave,Box 697, Rochester, NY 14642 USA

[2] Univ Sheffield, Med Sch, Sheffield Dermatol Res, Sheffield, England

[3] Keio Univ, Sch Med, Dept Dermatol, Tokyo, Japan

[4] RIKEN Ctr Integrat Med Sci, Lab Skin Homeostasis, Yokohama, Japan

[5] Kyoto Univ, Grad Sch Med, Dept Dermatol, Kyoto, Japan

[6] Regeneron Pharmaceut Inc, Tarrytown, NY USA

[7] Sanofi, Cambridge, MA USA

来源：

JID INNOVATIONS | 2022年 / 2卷 / 05期

关键词：

HUMAN STRATUM-CORNEUM; KERATIN INTERMEDIATE-FILAMENTS; DOWN-REGULATES FILAGGRIN; OF-FUNCTION MUTATIONS; STAPHYLOCOCCUS-AUREUS COLONIZATION; EPIDERMAL TIGHT-JUNCTIONS; SERINE-PROTEASE ACTIVITY; JANUS KINASE INHIBITOR; INNATE LYMPHOID-CELLS; COPY NUMBER VARIATION;

D O I：

10.1016/j.xjidi.2022.100131

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by hosteenvironment 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 inflammation therapies may improve dysfunctional skin barrier in AD.

引用

页数：20

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