Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis

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...

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Detalles Bibliográficos
Autores principales: Beck, Lisa A., Cork, Michael J., Amagai, Masayuki, De Benedetto, Anna, Kabashima, Kenji, Hamilton, Jennifer D., Rossi, Ana B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9428921/
https://www.ncbi.nlm.nih.gov/pubmed/36059592
http://dx.doi.org/10.1016/j.xjidi.2022.100131
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author Beck, Lisa A.
Cork, Michael J.
Amagai, Masayuki
De Benedetto, Anna
Kabashima, Kenji
Hamilton, Jennifer D.
Rossi, Ana B.
author_facet Beck, Lisa A.
Cork, Michael J.
Amagai, Masayuki
De Benedetto, Anna
Kabashima, Kenji
Hamilton, Jennifer D.
Rossi, Ana B.
author_sort Beck, Lisa A.
collection PubMed
description 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.
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spelling pubmed-94289212022-09-01 Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis Beck, Lisa A. Cork, Michael J. Amagai, Masayuki De Benedetto, Anna Kabashima, Kenji Hamilton, Jennifer D. Rossi, Ana B. JID Innov Review 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. Elsevier 2022-04-26 /pmc/articles/PMC9428921/ /pubmed/36059592 http://dx.doi.org/10.1016/j.xjidi.2022.100131 Text en © 2022 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review
Beck, Lisa A.
Cork, Michael J.
Amagai, Masayuki
De Benedetto, Anna
Kabashima, Kenji
Hamilton, Jennifer D.
Rossi, Ana B.
Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
title Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
title_full Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
title_fullStr Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
title_full_unstemmed Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
title_short Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
title_sort type 2 inflammation contributes to skin barrier dysfunction in atopic dermatitis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9428921/
https://www.ncbi.nlm.nih.gov/pubmed/36059592
http://dx.doi.org/10.1016/j.xjidi.2022.100131
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