Department of Human Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong Province, China ; Department of Human Anatomy, School of Basic Courses, Guangdong Pharmaceutical University, Guangzhou, Guangdong Province, China.
Department of Human Anatomy, School of Basic Courses, Guangdong Pharmaceutical University, Guangzhou, Guangdong Province, China.
Neural Regen Res. 2014 Aug 15;9(16):1541-7. doi: 10.4103/1673-5374.139481.
Alzheimer's disease is closely associated with disorders of neurogenesis in the brain, and growing evidence supports the involvement of immunological mechanisms in the development of the disease. However, at present, the role of T cells in neuronal regeneration in the brain is unknown. We injected amyloid-beta 1-42 peptide into the hippocampus of six BALB/c wild-type mice and six BALB/c-nude mice with T-cell immunodeficiency to establish an animal model of Alzheimer's disease. A further six mice of each genotype were injected with same volume of normal saline. Immunohistochemistry revealed that the number of regenerated neural progenitor cells in the hippocampus of BALB/c wild-type mice was significantly higher than that in BALB/c-nude mice. Quantitative fluorescence PCR assay showed that the expression levels of peripheral T cell-associated cytokines (interleukin-2, interferon-γ) and hippocampal microglia-related cytokines (interleukin-1β, tumor necrosis factor-α) correlated with the number of regenerated neural progenitor cells in the hippocampus. These results indicate that T cells promote hippocampal neurogenesis in Alzheimer's disease and T-cell immunodeficiency restricts neuronal regeneration in the hippocampus. The mechanism underlying the promotion of neuronal regeneration by T cells is mediated by an increased expression of peripheral T cells and central microglial cytokines in Alzheimer's disease mice. Our findings provide an experimental basis for understanding the role of T cells in Alzheimer's disease.
阿尔茨海默病与大脑中的神经发生障碍密切相关,越来越多的证据支持免疫机制参与疾病的发展。然而,目前 T 细胞在大脑神经元再生中的作用尚不清楚。我们将淀粉样β 1-42 肽注入 BALB/c 野生型和 T 细胞免疫缺陷 BALB/c 裸鼠的海马体中,建立阿尔茨海默病动物模型。每组基因型的另外 6 只小鼠注射相同体积的生理盐水。免疫组织化学显示,BALB/c 野生型小鼠海马体中再生神经祖细胞的数量明显高于 BALB/c 裸鼠。定量荧光 PCR 检测显示,外周 T 细胞相关细胞因子(白细胞介素-2、干扰素-γ)和海马微胶质细胞相关细胞因子(白细胞介素-1β、肿瘤坏死因子-α)的表达水平与海马体中再生神经祖细胞的数量相关。这些结果表明 T 细胞促进阿尔茨海默病中海马神经发生,而 T 细胞免疫缺陷限制海马体中的神经元再生。T 细胞促进神经元再生的机制是通过阿尔茨海默病小鼠外周 T 细胞和中枢微胶质细胞细胞因子的表达增加介导的。我们的发现为理解 T 细胞在阿尔茨海默病中的作用提供了实验依据。