Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Oct 10;13(20):3167. doi: 10.3390/diagnostics13203167

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Pathogenesis of AD. The primary components of the skin barrier are intercellular lipids in the stratum corneum, including ceramides. In addition, tight connections illustrate the adhesive structure between the epidermal cells which prevents foreign substrates from penetrating the skin. Chronic skin inflammation in AD is significantly affected by skin barrier dysfunction. Interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) are produced by epidermal keratinocytes and are responsible for type 2 immune response-mediated inflammation. Thymus- and activation-related chemokine (TARC) as well as macrophage-derived chemokine (MDC) are produced in atopic skin lesions and contribute to the migration of Th2 cells to skin lesions. IgE, immunoglobulin E.