Department of Anatomy, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria; College of Health Sciences, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Department of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria; College of Health Sciences, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Brain Res. 2023 Dec 15;1821:148589. doi: 10.1016/j.brainres.2023.148589. Epub 2023 Sep 20.
Alzheimer's disease, the leading cause of progressive cognitive decline globally, has been reported to be enhanced by neuroinflammation. Brain-resident innate immune cells and adaptive immune cells work together to produce neuroinflammation. Studies over the past decade have established the neuroimmune axis present in Alzheimer's disease; the crosstalk between adaptive and innate immune cells within and outside the brain is crucial to the onset and progression of Alzheimer's disease. Although the role of the adaptive immune system in Alzheimer's disease is not fully understood, it has been hypothesized that the brain's immune homeostasis is significantly disrupted, which greatly contributes to neuroinflammation. Brain-infiltrating T cells possess proinflammatory phenotypes and activities that directly contribute to neuroinflammation. The pro-inflammatory activities of the adaptive immune system in Alzheimer's disease are characterized by the upregulation of effector T cell activities and the downregulation of regulatory T cell activities in the brain, blood, and cerebrospinal fluid. In this review, we discuss the major impact of T lymphocytes on the pathogenesis and progression of Alzheimer's disease. Understanding the role and mechanism of action of T cells in Alzheimer's disease would significantly contribute to the identification of novel biomarkers for diagnosing and monitoring the progression of the disease. This knowledge could also be crucial to the development of immunotherapies for Alzheimer's disease.
阿尔茨海默病是全球导致进行性认知能力下降的主要原因，据报道，其与神经炎症有关。脑内固有免疫细胞和适应性免疫细胞协同作用产生神经炎症。过去十年的研究已经确立了阿尔茨海默病中的神经免疫轴；脑内和脑外适应性和固有免疫细胞之间的串扰对阿尔茨海默病的发病和进展至关重要。尽管适应性免疫系统在阿尔茨海默病中的作用尚未完全阐明，但有假设认为大脑的免疫稳态显著受到破坏，这极大地促成了神经炎症。脑浸润 T 细胞具有促炎表型和活性，直接导致神经炎症。阿尔茨海默病中适应性免疫系统的促炎活性表现为效应 T 细胞活性上调，以及脑、血液和脑脊液中调节性 T 细胞活性下调。在这篇综述中，我们讨论了 T 淋巴细胞对阿尔茨海默病发病机制和进展的主要影响。了解 T 细胞在阿尔茨海默病中的作用和作用机制将极大地有助于确定用于诊断和监测疾病进展的新型生物标志物。这一知识对于开发阿尔茨海默病的免疫疗法也可能至关重要。
