TPN10475 Constrains Effector T Lymphocytes Activation and Attenuates Experimental Autoimmune Encephalomyelitis Pathogenesis by Facilitating TGF-β Signal Transduction
文献类型：期刊论文
| 作者 | Wang, Chun4; Jiang, Xiangrui2,3 ; Lv, Jie4; Zhuang, Wei1,3,4; Xie, Ling4; Liu, Guangyu4; Saimaier, Kaidireya4; Han, Sanxing4; Shi, Changjie4; Hua, Qiuhong4
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| 刊名 | JOURNAL OF NEUROIMMUNE PHARMACOLOGY
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| 出版日期 | 2024-02-27 |
| 卷号 | 19期号:1页码:16 |
| ISSN号 | 1557-1890 |
| 关键词 | Experimental autoimmune encephalomyelitis TGF-beta signal transduction Effector CD4(+) T cells activation Th/Treg Cell migration |
| DOI | 10.1007/s11481-024-10109-x |
| 通讯作者 | Du, Changsheng(ducs2015@163.com) |
| 英文摘要 | Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) mediated by immune cells, in which auto-reactive CD4(+) T cells have been implicated as a major driver in the pathogenesis of the disease. In this study, we aimed to investigate whether the artemisinin derivative TPN10475 could alleviate experimental autoimmune encephalomyelitis (EAE), a commonly used animal model of MS and its possible mechanisms. TPN10475 effectively resisted the reduction of TGF-beta signal transduction induced by TCR stimulation, suppressed the activation and function of effector CD4(+) T cells in vitro, and restricted the differentiation of pathogenic Th1 and Th17 cells. It was also found to negatively regulate the inflammatory response in EAE by reducing the peripheral activation drive of auto-reactive helper T lymphocytes, inhibiting the migration of inflammatory cells into the CNS to attenuate EAE. The above results suggested that the upregulation of TGF-beta signal transduction may provide new ideas for the study of MS pathogenesis and have positive implications for the development of drugs for the treatment of autoimmune diseases. |
| WOS关键词 | MULTIPLE-SCLEROSIS ; CELL QUIESCENCE ; DIFFERENTIATION ; INFLAMMATION |
| 资助项目 | National Natural Science Foundation of China |
| WOS研究方向 | Neurosciences & Neurology ; Pharmacology & Pharmacy |
| 语种 | 英语 |
| 出版者 | SPRINGER |
| WOS记录号 | WOS:001171448200001 |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/309880]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Du, Changsheng |
| 作者单位 | 1.Chinese Acad Sci, Inst Biophys, CAS Ctr Excellence Biomacromolecules, Natl Lab Biomacromolecules, Beijing 100101, Peoples R China 2.Chinese Acad Sci, CAS Key Lab Receptor Res, Shanghai Inst Mat Med, 555 Zuchongzhi Rd, Shanghai 201203, Peoples R China 3.Univ Chinese Acad Sci, 19A Yuquan Rd, Beijing 100049, Peoples R China 4.Tongji Univ, Orthopaed Dept, Sch Life Sci & Technol, Key Lab Spine & Spinal Cord Injury Repair & Regene, Shanghai 200092, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wang, Chun,Jiang, Xiangrui,Lv, Jie,et al. TPN10475 Constrains Effector T Lymphocytes Activation and Attenuates Experimental Autoimmune Encephalomyelitis Pathogenesis by Facilitating TGF-β Signal Transduction[J]. JOURNAL OF NEUROIMMUNE PHARMACOLOGY,2024,19(1):16. |
| APA | Wang, Chun.,Jiang, Xiangrui.,Lv, Jie.,Zhuang, Wei.,Xie, Ling.,...&Du, Changsheng.(2024).TPN10475 Constrains Effector T Lymphocytes Activation and Attenuates Experimental Autoimmune Encephalomyelitis Pathogenesis by Facilitating TGF-β Signal Transduction.JOURNAL OF NEUROIMMUNE PHARMACOLOGY,19(1),16. |
| MLA | Wang, Chun,et al."TPN10475 Constrains Effector T Lymphocytes Activation and Attenuates Experimental Autoimmune Encephalomyelitis Pathogenesis by Facilitating TGF-β Signal Transduction".JOURNAL OF NEUROIMMUNE PHARMACOLOGY 19.1(2024):16. |
入库方式： OAI收割
来源：上海药物研究所
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