Photobiomodulation suppresses allergic contact dermatitis by inhibiting T-cell activation.
T cell activation
allergic contact dermatitis
inflammation
photobiomodulation
Journal
Contact dermatitis
ISSN: 1600-0536
Titre abrégé: Contact Dermatitis
Pays: England
ID NLM: 7604950
Informations de publication
Date de publication:
10 Oct 2024
10 Oct 2024
Historique:
revised:
21
09
2024
received:
23
02
2024
accepted:
28
09
2024
medline:
11
10
2024
pubmed:
11
10
2024
entrez:
11
10
2024
Statut:
aheadofprint
Résumé
Allergic contact dermatitis (ACD) is a dermal inflammatory disease caused by allergic reactions to substances that contact the skin. The hyperactivation of T cells plays an important role in its pathogenesis. Photobiomodulation (PBM) is an efficacious therapeutic approach for suppressing inflammatory diseases. This study aimed to evaluate the potentially beneficial role of PBM in ACD models and investigate its possible mechanisms. In this study, the ACD model of C57BL/6 mice was produced and treated with PBM, and the number of T cells was evaluated. In an in vitro study, naïve T cells were isolated and intervened with PBM. The markers of T cell activation were detected by flow cytometer. Transforming growth factor-β (TGF-β) and reactive oxygen species (ROS) were detected to investigate the mechanism. PBM effectively inhibited the inflammatory response by impeding the number of T cells in the ACD model. And in vitro studies showed that PBM could directly moderate the activation of naïve T cells and possess the capability to impede T cell activation via TGF-beta signaling pathway. Our finding elucidates the potential mechanism underlying the inhibitory effects of PBM in inflammatory diseases and furnishes a theoretical foundation for its clinical application.
Sections du résumé
BACKGROUND
BACKGROUND
Allergic contact dermatitis (ACD) is a dermal inflammatory disease caused by allergic reactions to substances that contact the skin. The hyperactivation of T cells plays an important role in its pathogenesis. Photobiomodulation (PBM) is an efficacious therapeutic approach for suppressing inflammatory diseases.
OBJECTIVE
OBJECTIVE
This study aimed to evaluate the potentially beneficial role of PBM in ACD models and investigate its possible mechanisms.
METHODS
METHODS
In this study, the ACD model of C57BL/6 mice was produced and treated with PBM, and the number of T cells was evaluated. In an in vitro study, naïve T cells were isolated and intervened with PBM. The markers of T cell activation were detected by flow cytometer. Transforming growth factor-β (TGF-β) and reactive oxygen species (ROS) were detected to investigate the mechanism.
RESULTS
RESULTS
PBM effectively inhibited the inflammatory response by impeding the number of T cells in the ACD model. And in vitro studies showed that PBM could directly moderate the activation of naïve T cells and possess the capability to impede T cell activation via TGF-beta signaling pathway.
CONCLUSION
CONCLUSIONS
Our finding elucidates the potential mechanism underlying the inhibitory effects of PBM in inflammatory diseases and furnishes a theoretical foundation for its clinical application.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Nature Science Foundation of China
ID : 82122015
Organisme : National Nature Science Foundation of China
ID : 81991504
Organisme : National Nature Science Foundation of China
ID : 81974149
Organisme : National Key R&D of Program of China
ID : 2022YFC2504200
Organisme : Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support
ID : ZYLX202121
Organisme : Innovation Research Team Project of Beijing Stomatological Hospital, Capital Medical University
ID : CXTD202202
Organisme : Beijing Municipal Administration of Hospitals' Ascent Plan
ID : DFL20181501
Organisme : Young Scientist Program Of Beijing Stomatological Hospital, Capital Medical University
ID : YSP202402
Organisme : Beijing Municipal Administration of Hospitals' Youth Programme
ID : QML20181501
Informations de copyright
© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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