Innate immune activation as cofactor in pemphigus disease manifestation.
caspases
desmoglein
inflammasomes
interleukin 1
pemphigus vulgaris
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2022
2022
Historique:
received:
17
03
2022
accepted:
28
06
2022
entrez:
5
8
2022
pubmed:
6
8
2022
medline:
9
8
2022
Statut:
epublish
Résumé
Molecular mechanisms underlying auto-antibody-induced acantholysis in pemphigus vulgaris are subject of current research to date. To decipher the discrepancy between ubiquitous antibody binding to the epidermal desmosomes, but discontinuous disease manifestation, we were able to identify Ultraviolet A (UVA) as a cofactor for acantholysis. UVA induces interleukin (IL)-1 secretion in keratinocytes, mirroring innate immune system activation. In an
Identifiants
pubmed: 35928825
doi: 10.3389/fimmu.2022.898819
pmc: PMC9343989
doi:
Substances chimiques
Immunoglobulin G
0
Caspases
EC 3.4.22.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
898819Informations de copyright
Copyright © 2022 Eichkorn, Schmidt, Walter, Hertl, Baron, Waschke and Yazdi.
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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