中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
The chemokine receptor antagonist, TAK-779, decreased experimental autoimmune encephalomyelitis by reducing inflammatory cell migration into the central nervous system, without affecting T cell function

文献类型:期刊论文

作者Ni, Jia1; Zhu, Yi-Na1; Zhong, Xiang-Gen1; Ding, Yu1; Hou, Li-Fei1; Tong, Xian-Kun1; Tang, Wei1; Ono, Shiro2; Yang, Yi-Fu1,3; Zuo, Jian-Ping1,3
刊名BRITISH JOURNAL OF PHARMACOLOGY
出版日期2009-12
卷号158期号:8页码:2046-2056
关键词experimental autoimmune encephalomyelitis CCR5 CXCR3 chemokine T cell migration
ISSN号0007-1188
DOI10.1111/j.1476-5381.2009.00528.x
文献子类Article
英文摘要Background and purpose: The C-C chemokine receptor CCR5, and the C-X-C chemokine receptor CXCR3 are involved in the regulation of T cell-mediated immune responses, and in the migration and activation of these cells. To determine whether blockade of these chemokine receptors modulated inflammatory responses in the central nervous sytem (CNS), we investigated the effect of a non-peptide chemokine receptor antagonist, TAK-779, in mice with experimental autoimmune encephalomyelitis (EAE). Experimental approach: EAE was induced by immunization of C57BL/6 mice with myelin oligodendrocyte glycoprotein (MOG) 35-55. TAK-779 was injected s.c. once a day after immunization. Disease incidence and severity (over 3 weeks) were monitored by histopathological evaluation and FACS assay of inflammatory cells infiltrating into the spinal cord, polymerase chain reaction quantification of mRNA expression, assay of T cell proliferation, by [3H]-thymidine incorporation and cytokine production by enzyme-linked immunosorbent assay. Key results: Treatment with TAK-779 reduced incidence and severity of EAE. It strongly inhibited migration of CXCR3/CCR5 bearing CD4+, CD8+ and CD11b+ leukocytes to the CNS. TAK-779 did not reduce proliferation of anti-MOG T cells, the production of IFN-gamma by T cells or CXCR3 expression on T cells. In addition, TAK-779 did not affect production of IL-12 by antigen-presenting cells, CCR5 induction on T cells and the potential of MOG-specific T cells to transfer EAE. Conclusions and implications: TAK-779 restricted the development of MOG-induced EAE. This effect involved reduced migration of inflammatory cells into the CNS without affecting responses of anti-MOG T cells or the ability of MOG-specific T cells to transfer EAE.
WOS关键词EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS ; NONPEPTIDE CCR5 ANTAGONIST ; COMPOUND TARGETING CCR5 ; IFN-GAMMA ; SMALL-MOLECULE ; MULTIPLE-SCLEROSIS ; EXPRESSION ; CXCR3 ; MICE ; INDUCTION
资助项目Shanghai Science and Technology Committee[08XD14053] ; Shanghai Science and Technology Committee[08DZ1980200] ; Shanghai Science and Technology Committee[064319014]
WOS研究方向Pharmacology & Pharmacy
语种英语
WOS记录号WOS:000272569100020
出版者WILEY
源URL[http://119.78.100.183/handle/2S10ELR8/279071]  
专题药理学第一研究室
中科院受体结构与功能重点实验室
新药研究国家重点实验室
通讯作者Zuo, Jian-Ping
作者单位1.Chinese Acad Sci, Shanghai Inst Mat Med, Lab Immunopharmacol, State Key Lab Drug Res, Shanghai 201203, Peoples R China;
2.Osaka Ohtani Univ, Immunol Lab, Fac Pharm, Osaka, Japan;
3.Shanghai Univ Tradit Chinese Med, Lab Immunol & Virol, Shanghai, Peoples R China
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Ni, Jia,Zhu, Yi-Na,Zhong, Xiang-Gen,et al. The chemokine receptor antagonist, TAK-779, decreased experimental autoimmune encephalomyelitis by reducing inflammatory cell migration into the central nervous system, without affecting T cell function[J]. BRITISH JOURNAL OF PHARMACOLOGY,2009,158(8):2046-2056.
APA Ni, Jia.,Zhu, Yi-Na.,Zhong, Xiang-Gen.,Ding, Yu.,Hou, Li-Fei.,...&Zuo, Jian-Ping.(2009).The chemokine receptor antagonist, TAK-779, decreased experimental autoimmune encephalomyelitis by reducing inflammatory cell migration into the central nervous system, without affecting T cell function.BRITISH JOURNAL OF PHARMACOLOGY,158(8),2046-2056.
MLA Ni, Jia,et al."The chemokine receptor antagonist, TAK-779, decreased experimental autoimmune encephalomyelitis by reducing inflammatory cell migration into the central nervous system, without affecting T cell function".BRITISH JOURNAL OF PHARMACOLOGY 158.8(2009):2046-2056.

入库方式: OAI收割

来源:上海药物研究所

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