Contact dermatitis · 2024
Photobiomodulation suppresses allergic contact dermatitis by inhibiting T-cell activation.
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Fu Jingfei, Zhao Rui, Jiang Yiyang, Chen Yingyi, Du Juan, Liu Yi, Xu Junji
Аннотация
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: This study aimed to evaluate the potentially beneficial role of PBM in ACD models and investigate its possible mechanisms.
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: 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: Our finding elucidates the potential mechanism underlying the inhibitory effects of PBM in inflammatory diseases and furnishes a theoretical foundation for its clinical application.
OBJECTIVE: This study aimed to evaluate the potentially beneficial role of PBM in ACD models and investigate its possible mechanisms.
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: 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: Our finding elucidates the potential mechanism underlying the inhibitory effects of PBM in inflammatory diseases and furnishes a theoretical foundation for its clinical application.