Department of Neurology, Methodist Neurological Institute, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, TX, USA.
Trends Immunol. 2010 Jan;31(1):7-17. doi: 10.1016/j.it.2009.09.003. Epub 2009 Oct 31.
Neuroinflammation is a pathological hallmark in Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), and is characterized by activated microglia and infiltrating T cells at sites of neuronal injury. In PD and ALS, neurons do not die alone; neuronal injury is non-cell-autonomous and depends on a well-orchestrated dialogue in which neuronally secreted misfolded proteins activate microglia and initiate a self-propagating cycle of neurotoxicity. Diverse populations and phenotypes of CD4(+) T cells crosstalk with microglia, and depending on their activation status, influence this dialogue and promote neuroprotection or neurotoxicity. A greater understanding of the T cell population that mediates these effects, as well as the molecular signals involved should provide targets for neuroprotective immunomodulation to treat these devastating neurodegenerative diseases.
神经炎症是帕金森病（PD）和肌萎缩性侧索硬化症（ALS）的病理标志，其特征是神经元损伤部位的小胶质细胞和浸润的 T 细胞被激活。在 PD 和 ALS 中，神经元不会单独死亡；神经元损伤是非细胞自主的，并取决于精心协调的对话，在这种对话中，神经元分泌的错误折叠蛋白激活小胶质细胞并引发自我传播的神经毒性循环。不同群体和表型的 CD4(+) T 细胞与小胶质细胞相互作用，并且根据其激活状态，影响这种对话并促进神经保护或神经毒性。更深入地了解介导这些效应的 T 细胞群体以及涉及的分子信号，应该为神经保护性免疫调节提供治疗这些毁灭性神经退行性疾病的靶点。
