Huang Zhi, Ha Grace K, Petitto John M
Recent Res Dev Neurosci. 2013;4:109-119.
The proneuronal effects of T cells that impact the brain occur from both T cells trafficking into the brain, and from signals in the periphery (e.g., cytokine release and regulation). Recent data indicates that neuroimmunological changes in the brain can modify intrinsic brain processes that are involved in regulating neuroplasticity (e.g., T-cell/microglial interactions, neurotrophins, neurogenesis). We describe: 1) work from our lab and others showing that injury-induced loss of neuronal phenotype and reversal of motor neuron atrophy are associated with normal T cell immunity, and; 2) research indicating that these and other neuroimmunological processes may be generalizable to mechanisms of neuroplasticity involved in cognitive and emotional behavior. These findings are discussed in relation to our lab's working hypothesis, that T cell immunosenesence may contribute to alterations in brain neuroplasticity related to aging. Greater understanding of the role of adaptive T cell immunity on neuroplasticity could have important clinical implications for developing novel treatment strategies for neurodegenerative diseases (e.g., Alzheimer's) and brain injury (e.g., stroke, trauma).
影响大脑的T细胞的促神经元效应既源于进入大脑的T细胞,也源于外周的信号(如细胞因子释放和调节)。最近的数据表明,大脑中的神经免疫变化可以改变参与调节神经可塑性的内在大脑过程(如T细胞/小胶质细胞相互作用、神经营养因子、神经发生)。我们描述:1)我们实验室和其他实验室的研究表明,损伤诱导的神经元表型丧失和运动神经元萎缩的逆转与正常T细胞免疫有关;2)研究表明,这些以及其他神经免疫过程可能适用于参与认知和情感行为的神经可塑性机制。这些发现与我们实验室的工作假设相关,即T细胞免疫衰老可能导致与衰老相关的大脑神经可塑性改变。深入了解适应性T细胞免疫在神经可塑性中的作用,可能对开发神经退行性疾病(如阿尔茨海默病)和脑损伤(如中风、创伤)的新治疗策略具有重要的临床意义。