Aurintricarboxylic Acid Ameliorates Experimental Autoimmune Encephalomyelitis by Blocking Chemokine-Mediated Pathogenic Cell Migration and Infiltration

doi:10.4049/jimmunol.1201994

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	Aurintricarboxylic Acid Ameliorates Experimental Autoimmune Encephalomyelitis by Blocking Chemokine-Mediated Pathogenic Cell Migration and Infiltration
	Zhang, Feifei 2; Wei, Wei 2; Chai, Hui 2; Xie, Xin1,2
刊名	JOURNAL OF IMMUNOLOGY
	2013-02-01
卷号	190 期号:3 页码:1017-1025
ISSN号	0022-1767
DOI	10.4049/jimmunol.1201994
文献子类	Article
英文摘要	Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune diseases characterized by the immune-mediated demyelination and neurodegeneration of the CNS. Overactivation of CD4(+) T cells, especially the Th1 and Th17 subpopulations, is thought to be the direct cause of this disease. Aurintricarboxylic acid (ATA), an inhibitor of protein-nucleic acid interaction, has been reported to block with the JAK/STAT signaling pathway that is critical for Th cell differentiation. In this study, we discovered that ATA treatment significantly reduces the clinical score of EAE, but it does not directly inhibit the differentiation of Th1 and Th17 cells in vitro. ATA was found to block the chemotaxis and accumulation of dendritic cells in the spleen of EAE mice before the onset of the disease and to reduce the percentage of Th1 and Th17 cells in the spleen. Further study revealed that ATA also blocks the infiltration of pathogenic T cells into the CNS and blocks the onset of passive EAE. ATA was found to inhibit the functions of many chemokine receptors. By blocking chemokine-mediated migration of dendritic cells and pathogenic T cells, ATA alleviates the pathogenesis of EAE and might be used to treat autoimmune diseases, including multiple sclerosis. The Journal of Immunology, 2013, 190: 1017-1025.
资助项目	Chinese Academy of Sciences[XDA01040301] ; Ministry of Science and Technology of China[2009CB940900] ; Ministry of Science and Technology of China[2012ZX09301001-005] ; Shanghai Commission of Science and Technology[12XD1402100] ; Shanghai Commission of Science and Technology[11DZ2292200]
WOS关键词	BLOOD-BRAIN-BARRIER ; PROTEIN-COUPLED RECEPTORS ; HELPER T-CELLS ; DENDRITIC CELL ; MULTIPLE-SCLEROSIS ; T-H-17 CELLS ; HIV-1 ; TRAFFICKING ; VIRUS ; STAT3
WOS研究方向	Immunology
语种	英语
出版者	AMER ASSOC IMMUNOLOGISTS
WOS记录号	WOS:000313784200020
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/277750]
专题	国家新药筛选中心
通讯作者	Xie, Xin
作者单位	1.Tongji Univ, Sch Life Sci & Technol, Lab Receptor Based Biomed, Shanghai Key Lab Signaling & Dis Res, Shanghai 200092, Peoples R China 2.Chinese Acad Sci, Shanghai Inst Mat Med, Natl Ctr Drug Screening, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China;
推荐引用方式 GB/T 7714	Zhang, Feifei,Wei, Wei,Chai, Hui,et al. Aurintricarboxylic Acid Ameliorates Experimental Autoimmune Encephalomyelitis by Blocking Chemokine-Mediated Pathogenic Cell Migration and Infiltration[J]. JOURNAL OF IMMUNOLOGY,2013,190(3):1017-1025.
APA	Zhang, Feifei,Wei, Wei,Chai, Hui,&Xie, Xin.(2013).Aurintricarboxylic Acid Ameliorates Experimental Autoimmune Encephalomyelitis by Blocking Chemokine-Mediated Pathogenic Cell Migration and Infiltration.JOURNAL OF IMMUNOLOGY,190(3),1017-1025.
MLA	Zhang, Feifei,et al."Aurintricarboxylic Acid Ameliorates Experimental Autoimmune Encephalomyelitis by Blocking Chemokine-Mediated Pathogenic Cell Migration and Infiltration".JOURNAL OF IMMUNOLOGY 190.3(2013):1017-1025.