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首页> 外文期刊>Neuron >Neuronal damage in autoimmune neuroinflammation mediated by the death ligand TRAIL.
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Neuronal damage in autoimmune neuroinflammation mediated by the death ligand TRAIL.

机译：死亡配体TRAIL介导的自身免疫性神经炎症中的神经元损伤。

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Here, we provide evidence for a detrimental role of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in neural death in T cell-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Clinical severity and neuronal apoptosis in brainstem motor areas were substantially reduced upon brain-specific blockade of TRAIL after induction of EAE through adoptive transfer of encephalitogenic T cells. Furthermore, TRAIL-deficient myelin-specific lymphocytes showed reduced encephalitogenicity when transferred to wild-type mice. Conversely, intracerebral delivery of TRAIL to animals with EAE increased clinical deficits, while naive mice were not susceptible to TRAIL. Using organotypic slice cultures as a model for living brain tissue, we found that neurons were susceptible to TRAIL-mediated injury induced by encephalitogenic T cells. Thus, in addition to its known immunoregulatory effects, the death ligand TRAIL contributes to neural damage in the inflamed brain.
机译：在这里，我们提供证据证明肿瘤坏死因子相关的凋亡诱导配体（TRAIL）在T细胞诱导的实验性自身免疫性脑脊髓炎（EAE）（一种多发性硬化症（MS）的动物模型）的神经死亡中具有有害作用。通过过继转移脑致病性T细胞诱导EAE后，通过脑特异性阻滞TRAIL，脑干运动区的临床严重程度和神经元凋亡大大降低。此外，TRAIL缺乏的髓鞘特异性淋巴细胞转移到野生型小鼠时显示出减少的致脑病作用。相反，向具有EAE的动物脑内运输TRAIL会增加临床缺陷，而幼稚的小鼠对TRAIL不敏感。使用器官切片培养物作为活脑组织的模型，我们发现神经元易受致脑病性T细胞诱导的TRAIL介导的损伤。因此，除其已知的免疫调节作用外，死亡配体TRAIL有助于发炎的大脑中的神经损伤。

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