期刊
BRAIN
卷 133, 期 -, 页码 2248-2263出版社
OXFORD UNIV PRESS
DOI: 10.1093/brain/awq179
关键词
axonal damage; experimental autoimmune encephalomyelitis; neurotrophin
资金
- Gemeinnutzige Hertie-Stiftung [AZ 1.01.1/05/009]
- Gemeinnutzige Hertie-Stiftung (Bonn, IMSF)
- EU [LSHM-CT-2005-018637]
- Walter-und Ilse-Rose Foundation
- Deutsche Forschungsgemeinschaft (DFG) [FOR1336, A2, B1, SFB 581, TP A1, B4]
- BMBF
Brain-derived neurotrophic factor plays a key role in neuronal and axonal survival. Brain-derived neurotrophic factor is expressed in the immune cells in lesions of experimental autoimmune encephalomyelitis and multiple sclerosis, thus potentially mediating neuroprotective effects. We investigated the functional role of brain-derived neurotrophic factor in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Mice deficient for brain-derived neurotrophic factor in immune cells displayed an attenuated immune response in the acute phase of experimental autoimmune encephalomyelitis, but progressive disability with enhanced axonal loss in the chronic phase of the disease. In mice deficient for central nervous system-derived brain-derived neurotrophic factor via glial fibrillary acidic protein-crescentin-mediated deletion, a more severe course of experimental autoimmune encephalomyelitis and an overall increased axonal loss was observed. In a lentiviral approach, injection of brain-derived neurotrophic factor-overexpressing T cells led to a less severe course of experimental autoimmune encephalomyelitis and direct axonal protection. Our data imply a functional role of brain-derived neurotrophic factor in autoimmune demyelination by mediating axon protection.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据