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

文献类型：期刊论文

作者Liu, Guangyu6; Jiang, Xiangrui1,4; Han, Mengyao6; Lv, Jie6; Zhuang, Wei4,5,6; Xie, Ling6; Zhang, Yan2,4; Wang, Chun6; Saimaier, Kaidireya6; Yang, Jingshu3
刊名CELLULAR IMMUNOLOGY
出版日期2022-03-01
卷号373页码:10
关键词EAE Cell migration Th1 Th17 differentiation
ISSN号0008-8749
DOI10.1016/j.cellimm.2022.104500
通讯作者Shen, Jingshan(shenjingshan@simm.ac.cn) ; Li, Ning(lining_hs@fudan.edu.cn) ; Du, Changsheng(ducs2015@163.com)
英文摘要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.
WOS关键词CENTRAL-NERVOUS-SYSTEM ; CD4(+) T-CELLS ; CHEMOKINE RECEPTORS ; SURFACE EXPRESSION ; CC-CHEMOKINE ; RHO-GTPASES ; INFILTRATION ; MECHANISMS ; ARTESUNATE ; MONOCYTES
资助项目National Natural Science Foundation of China[32070768] ; National Natural Science Foundation of China[31871404] ; National Natural Science Foundation of China[31900658]
WOS研究方向Cell Biology ; Immunology
语种英语
WOS记录号WOS:000802190500003
出版者ACADEMIC PRESS INC ELSEVIER SCIENCE
源URL[http://119.78.100.183/handle/2S10ELR8/301298]  
专题中国科学院上海药物研究所
通讯作者Shen, Jingshan; Li, Ning; Du, Changsheng
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, 555 Zuchongzhi Rd, Shanghai 201203, Peoples R China
2.Chinese Acad Sci, Xinjiang Tech Inst Phys & Chem, 40-1 Beijing Rd, Urumqi 830011, Xinjiang, Peoples R China
3.Fudan Univ, Huashan Hosp, Natl Med Ctr Infect Dis, Dept Infect Dis,Shanghai Key Lab Infect Dis & Bio, Shanghai 200040, Peoples R China
4.Univ Chinese Acad Sci, 19A Yuquan Rd, Beijing 100049, Peoples R China
5.Chinese Acad Sci, Inst Biophys, CAS Ctr Excellence Biomacromol, Natl Lab Biomacromol, Beijing 100101, Peoples R China
6.Tongji Univ, Orthopaed Dept Tongji Hosp, Sch Life Sci & Technol, Key Lab Spine & Spinal Cord Injury Repair & Regen, Shanghai 200092, Peoples R China
推荐引用方式
GB/T 7714		 Liu, Guangyu,Jiang, Xiangrui,Han, Mengyao,et al. Artemisinin derivative TPN10466 suppresses immune cell migration and Th1/Th17 differentiation to ameliorate disease severity in experimental autoimmune encephalomyelitis[J]. CELLULAR IMMUNOLOGY,2022,373:10.
APA Liu, Guangyu.,Jiang, Xiangrui.,Han, Mengyao.,Lv, Jie.,Zhuang, Wei.,...&Du, Changsheng.(2022).Artemisinin derivative TPN10466 suppresses immune cell migration and Th1/Th17 differentiation to ameliorate disease severity in experimental autoimmune encephalomyelitis.CELLULAR IMMUNOLOGY,373,10.
MLA Liu, Guangyu,et al."Artemisinin derivative TPN10466 suppresses immune cell migration and Th1/Th17 differentiation to ameliorate disease severity in experimental autoimmune encephalomyelitis".CELLULAR IMMUNOLOGY 373(2022):10.

入库方式： OAI收割

来源：上海药物研究所

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