Regulatory T (Treg) cells interact with a variety of resident cells and infiltrated immune cells in the central nervous system (CNS) to modulate neuroinflammation and neurodegeneration. Extracellular amyloid-β (Aβ) peptide deposition and secondary persistent inflammation due to activation of microglia, astrocytes, and infiltrated immune cells contribute to Alzheimer's disease (AD)-related neurodegeneration. The majority of evidence supports the neuroprotective effects of Treg cells in AD. In the early stages of AD, appropriate Treg cell activity is required for the induction of microglia and astrocyte phagocytic activity in order to clear A deposits and prevent neuroinflammation. Such neuroprotective impacts were in part attributed to the ability of Treg cells to suppress deleterious and/or boost beneficial functions of microglia/astrocytes. In the later stages of AD, an effective Treg cell activity needs to prevent neurotoxicity and neurodegeneration. Treg cells can exert preventive effects on Th1-, and Th17 cell-related pathologic responses, whilst potentiating Th2-mediated protective activity. The impaired Treg cell-related immunomodulatory mechanisms have been described in AD patients and in related animal models which can contribute to the onset and progression of AD. This review aimed to provide a comprehensive figure regarding the role of Treg cells in AD while highlighting potential therapeutic approaches.

调节性 T (Treg) 细胞与中枢神经系统 (CNS) 中的各种常驻细胞和浸润性免疫细胞相互作用，调节神经炎症和神经变性。由于小胶质细胞、星形胶质细胞和浸润免疫细胞的激活，细胞外淀粉样蛋白-β (Aβ) 肽沉积和继发性持续炎症会导致阿尔茨海默病 (AD) 相关的神经变性。大多数证据支持 Treg 细胞在 AD 中的神经保护作用。在AD的早期阶段，需要适当的Treg细胞活性来诱导小胶质细胞和星形胶质细胞的吞噬活性，以清除A沉积物并预防神经炎症。这种神经保护作用部分归因于 Treg 细胞抑制小胶质细胞/星形胶质细胞的有害功能和/或增强有益功能的能力。在AD的后期，有效的Treg细胞活性需要预防神经毒性和神经变性。Treg 细胞可以对 Th1 和 Th17 细胞相关的病理反应发挥预防作用，同时增强 Th2 介导的保护活性。AD 患者和相关动物模型中已描述了 Treg 细胞相关免疫调节机制受损，这可能导致 AD 的发病和进展。本综述旨在提供有关 Treg 细胞在 AD 中的作用的全面数据，同时强调潜在的治疗方法。