Essential role of STAT3 signaling in hair follicle homeostasis
File(s)
Published version
Author(s)
Type
Journal Article
Abstract
Dominant-negative mutations associated with signal transducer and activator of transcription 3 (STAT3) signaling, which controls epithelial proliferation in various tissues, lead to atopic dermatitis in hyper IgE syndrome. This dermatitis is thought to be attributed to defects in STAT3 signaling in type 17 helper T cell specification. However, the role of STAT3 signaling in skin epithelial cells remains unclear. We found that STAT3 signaling in keratinocytes is required to maintain skin homeostasis by negatively controlling the expression of hair follicle-specific keratin genes. These expression patterns correlated with the onset of dermatitis, which was observed in specific pathogen-free conditions but not in germ-free conditions, suggesting the involvement of Toll-like receptor-mediated inflammatory responses. Thus, our study suggests that STAT3-dependent gene expression in keratinocytes plays a critical role in maintaining the homeostasis of skin, which is constantly exposed to microorganisms.
Date Issued
2021-11-11
Date Acceptance
2021-10-25
Citation
Frontiers in Immunology, 2021, 12
ISSN
1664-3224
Publisher
Frontiers Media
Journal / Book Title
Frontiers in Immunology
Volume
12
Copyright Statement
© 2021 Miyauchi, Ki, Ukai, Suzuki, Inoue, Suda, Matsui, Ito, Honda, Koseki, Ohara, Tanaka, Okada-Hatakeyama and Kubo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
License URL
Identifier
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2021.663177/full
Publication Status
Published
Article Number
663177
Date Publish Online
2021-11-11