Artemisinin derivative TPN10466 suppresses immune cell migration and Th1/Th17 differentiation to ameliorate disease severity in experimental autoimmune encephalomyelitis

•TPN10466 suppresses immune cell migration.•TPN10466 suppresses Th1/Th17 differentiation.•TPN10466 ameliorate disease severity in EAE. Multiple sclerosis (MS) was one of the major conditions causing neurological dysfunction and was an incurable progressive central nervous system disease. Experimenta...

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Published in:Cellular immunology 2022-03, Vol.373, p.104500-104500, Article 104500
Main Authors: Liu, Guangyu, Jiang, Xiangrui, Han, Mengyao, Lv, Jie, Zhuang, Wei, Xie, Ling, Zhang, Yan, Wang, Chun, Saimaier, Kaidireya, Yang, Jingshu, Shen, Jingshan, Li, Ning, Du, Changsheng
Format: Article
Language:English
Subjects:
Animals
Artemisinins - metabolism
Artemisinins - pharmacology
Artemisinins - therapeutic use
Cell Differentiation
Cell migration
Cell Movement
EAE
Encephalomyelitis, Autoimmune, Experimental
Mice
Mice, Inbred C57BL
Multiple Sclerosis - drug therapy
Multiple Sclerosis - metabolism
Severity of Illness Index
Th1 Cells
Th1/Th17 differentiation
Th17 Cells
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Summary:•TPN10466 suppresses immune cell migration.•TPN10466 suppresses Th1/Th17 differentiation.•TPN10466 ameliorate disease severity in EAE. Multiple sclerosis (MS) was one of the major conditions causing neurological dysfunction and was an incurable progressive central nervous system disease. Experimental autoimmune encephalomyelitis (EAE) was the most commonly used experimental model of MS. Artemisinin have been shown to exhibit anti-inflammatory effects through unclear mechanisms. In this study, we aimed to evaluate the effect of administration of the artemisinin derivative TPN10466 in EAE. TPN10466 alleviated the severity of disease in EAE. Further studies showed that TPN10466 inhibited lymphocyte migration by downregulating chemokine expression and adhesion molecules. In addition, studies showed that TPN10466 directly inhibited Th1 and Th17 differentiation and reduced Th1 and Th17 infiltration into the central nervous system. In conclusion, our work demonstrated that TPN10466 provided protection against the autoimmune disease EAE by inhibiting the migration of immune cells and suppressing Th1/Th17 differentiation, suggesting that TPN10466 could be a potential for promising potential agent for the treatment of MS/EAE.
ISSN:0008-8749
1090-2163
DOI:10.1016/j.cellimm.2022.104500