JAK/STAT Inhibition Normalizes Lipid Composition in 3D Human Epidermal Equivalents Challenged with Th2 Cytokines.
Humans
Th2 Cells
/ metabolism
STAT Transcription Factors
/ metabolism
Janus Kinases
/ metabolism
Cytokines
/ metabolism
Lipid Metabolism
/ drug effects
Epidermis
/ metabolism
Signal Transduction
/ drug effects
Piperidines
/ pharmacology
Pyrimidines
/ pharmacology
Janus Kinase Inhibitors
/ pharmacology
Interleukin-4
/ metabolism
Fatty Acids
/ metabolism
3D skin model
JAK/STAT
Th2 cytokines
atopic dermatitis
skin lipidomics
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
29 Apr 2024
29 Apr 2024
Historique:
received:
27
03
2024
revised:
23
04
2024
accepted:
24
04
2024
medline:
10
5
2024
pubmed:
10
5
2024
entrez:
10
5
2024
Statut:
epublish
Résumé
Derangement of the epidermal barrier lipids and dysregulated immune responses are key pathogenic features of atopic dermatitis (AD). The Th2-type cytokines interleukin IL-4 and IL-13 play a prominent role in AD by activating the Janus Kinase/Signal Transduction and Activator of Transcription (JAK/STAT) intracellular signaling axis. This study aimed to investigate the role of JAK/STAT in the lipid perturbations induced by Th2 signaling in 3D epidermal equivalents. Tofacitinib, a low-molecular-mass JAK inhibitor, was used to screen for JAK/STAT-mediated deregulation of lipid metabolism. Th2 cytokines decreased the expression of
Identifiants
pubmed: 38727296
pii: cells13090760
doi: 10.3390/cells13090760
pii:
doi:
Substances chimiques
STAT Transcription Factors
0
Janus Kinases
EC 2.7.10.2
Cytokines
0
tofacitinib
87LA6FU830
Piperidines
0
Pyrimidines
0
Janus Kinase Inhibitors
0
Interleukin-4
207137-56-2
Fatty Acids
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Pfizer (United States)
ID : ID69352343