神经炎症
FOXP3型
免疫系统
脉络丛
免疫学
医学
免疫抑制
小胶质细胞
调节性T细胞
疾病
神经科学
T细胞
生物
白细胞介素2受体
病理
炎症
中枢神经系统
作者
Kuti Baruch,Neta Rosenzweig,Alexander Kertser,Aleksandra Deczkowska,Alaa Sharif,Amit Spinrad,Afroditi Tsitsou-Kampeli,Ayelet Sarel,Liora Cahalon,Michal Schwartz
摘要
Alzheimer's disease (AD) is a neurodegenerative disorder in which chronic neuroinflammation contributes to disease escalation. Nevertheless, while immunosuppressive drugs have repeatedly failed in treating this disease, recruitment of myeloid cells to the CNS was shown to play a reparative role in animal models. Here we show, using the 5XFAD AD mouse model, that transient depletion of Foxp3(+) regulatory T cells (Tregs), or pharmacological inhibition of their activity, is followed by amyloid-β plaque clearance, mitigation of the neuroinflammatory response and reversal of cognitive decline. We further show that transient Treg depletion affects the brain's choroid plexus, a selective gateway for immune cell trafficking to the CNS, and is associated with subsequent recruitment of immunoregulatory cells, including monocyte-derived macrophages and Tregs, to cerebral sites of plaque pathology. Our findings suggest targeting Treg-mediated systemic immunosuppression for treating AD.
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