CD4+ T cells from Copolymer-1 immunized mice protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease
CD4+ T cells from Copolymer-1 immunized mice protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease
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DOI：
10.1016/j.jneuroim.2006.11.009
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发表时间：
2007-02-01
影响因子：
3.3
通讯作者：
Mosley, R. Lee
中科院分区：
文献类型：
--
作者：
Laurie, Chad;Reynolds, Ashley;Mosley, R. Lee
来自共聚物1（Cop-1）免疫小鼠的淋巴细胞的连续转移导致黑质内的T细胞积累、小胶质细胞应答的调节、胶质细胞衍生的神经营养因子的上调以及1-甲基-4-苯基-1，2，3，6-四氢吡啶（MPTP）中毒后黑质纹状体的保护。我们现在证明，从Cop-1免疫动物的淋巴结和脾脏中分离的T细胞以剂量依赖性方式保护黑质纹状体系统免受MPTP诱导的神经变性。CD 4 + T细胞引起最显著的神经保护反应，而高滴度的抗Cop-1抗体没有显示出效果。这些数据进一步支持使用免疫调节策略治疗帕金森病。(c)2006年由Elsevier B. V.出版
Adoptive transfer of lymphoid cells from Copolymer 1 (Cop-1) immunized mice leads to T cell accumulation within the substantia nigra, modulation of microglial responses, upregulation of glial cell derived neurotrophic factor, and protection of the nigrostriatum following 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP) intoxication. We now demonstrate that T cells isolated from lymph nodes and spleens of Cop-1 immunized animals protect the nigrostriatal system from MPTP-induced neurodegeneration in a dose-dependent manner. CD4+ T cells elicited the most significant neuroprotective response while high titers of anti-Cop-1 antibodies showed no effect. These data further support the use of immunomodulatory strategies for Parkinson's disease. (c) 2006 Published by Elsevier B.V.