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
Descripción
Sumario: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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