Interleukin 17 Promotes Expression of Alarmins S100A8 and S100A9 During the Inflammatory Response of Keratinocytes.
S100A8
MRP14
MRP8
S100A9
calprotectin
keratinocytes
myeloid-related proteins
psoriasis
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
28
08
2020
accepted:
22
12
2020
entrez:
1
3
2021
pubmed:
2
3
2021
medline:
17
6
2021
Statut:
epublish
Résumé
Psoriasis is one of the most common immune-mediated inflammatory skin diseases. Expression and secretion of two pro-inflammatory molecules of the S100-alarmin family, S100A8 and S100A9, in keratinocytes is a hallmark of psoriasis, which is also characterized by an altered differentiation of keratinocytes. Dimers of S100A8/S100A9 (calprotectin) bind to Toll-like receptor 4 and induce an inflammatory response in target cells. Targeted deletion of S100A9 reduced the inflammatory phenotype of psoriasis-like inflammation in mice. A role of S100-alarmins in differentiation and activation of keratinocytes was suggested but has been never shown in primary keratinocytes. We now confirm that induction of S100-alarmins in an imiquimod-induced murine model of psoriasis-like skin inflammation was associated with an increased expression of interleukin (IL)-1α, IL-6, IL-17A, or TNFα. This association was confirmed in transcriptome data obtained from controls, lesional and non-lesional skin of psoriasis patients, and a down-regulation of S100-alarmin expression after IL-17 directed therapy. However, analyzing primary S100A9
Identifiants
pubmed: 33643287
doi: 10.3389/fimmu.2020.599947
pmc: PMC7906991
doi:
Substances chimiques
Calgranulin A
0
Calgranulin B
0
Il17a protein, mouse
0
Il17f protein, mouse
0
Interleukin-17
0
S100A9 protein, mouse
0
S100a8 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
599947Informations de copyright
Copyright © 2021 Christmann, Zenker, Martens, Hübner, Loser, Vogl and Roth.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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