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The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis

Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by inflammatory cell skin infiltration. The JAK-STAT pathway has been shown to play an essential role in the dysregulation of immune responses in AD, including the exaggeration of Th2 cell response, the activation o...

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Detalles Bibliográficos
Autores principales: Bao, Lei, Zhang, Huayi, Chan, Lawrence S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772104/
https://www.ncbi.nlm.nih.gov/pubmed/24069552
http://dx.doi.org/10.4161/jkst.24137
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author Bao, Lei
Zhang, Huayi
Chan, Lawrence S
author_facet Bao, Lei
Zhang, Huayi
Chan, Lawrence S
author_sort Bao, Lei
collection PubMed
description Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by inflammatory cell skin infiltration. The JAK-STAT pathway has been shown to play an essential role in the dysregulation of immune responses in AD, including the exaggeration of Th2 cell response, the activation of eosinophils, the maturation of B cells, and the suppression of regulatory T cells (Tregs). In addition, the JAK-STAT pathway, activated by IL-4, also plays a critical role in the pathogenesis of AD by upregulating epidermal chemokines, pro-inflammatroy cytokines, and pro-angiogenic factors as well as by downregulating antimicrobial peptides (AMPs) and factors responsible for skin barrier function. In this review, we will highlight the recent advances in our understanding of the JAK-STAT pathway in the pathogenesis of AD.
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spelling pubmed-37721042013-09-25 The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis Bao, Lei Zhang, Huayi Chan, Lawrence S JAKSTAT Review Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by inflammatory cell skin infiltration. The JAK-STAT pathway has been shown to play an essential role in the dysregulation of immune responses in AD, including the exaggeration of Th2 cell response, the activation of eosinophils, the maturation of B cells, and the suppression of regulatory T cells (Tregs). In addition, the JAK-STAT pathway, activated by IL-4, also plays a critical role in the pathogenesis of AD by upregulating epidermal chemokines, pro-inflammatroy cytokines, and pro-angiogenic factors as well as by downregulating antimicrobial peptides (AMPs) and factors responsible for skin barrier function. In this review, we will highlight the recent advances in our understanding of the JAK-STAT pathway in the pathogenesis of AD. Landes Bioscience 2013-07-01 2013-08-15 /pmc/articles/PMC3772104/ /pubmed/24069552 http://dx.doi.org/10.4161/jkst.24137 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Review
Bao, Lei
Zhang, Huayi
Chan, Lawrence S
The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
title The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
title_full The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
title_fullStr The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
title_full_unstemmed The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
title_short The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
title_sort involvement of the jak-stat signaling pathway in chronic inflammatory skin disease atopic dermatitis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772104/
https://www.ncbi.nlm.nih.gov/pubmed/24069552
http://dx.doi.org/10.4161/jkst.24137
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