在脂多糖诱导的神经炎症和3xTg阿尔茨海默病模型中，CX3CR1转导的调节性T细胞归巢至前脑的过继转移

Adoptive Transfer of CX3CR1-Transduced Tregs Homing to the Forebrain in Lipopolysaccharide-Induced Neuroinflammation and 3xTg Alzheimer's Disease Models.

作者信息

Yang Hyejin, Yang Juwon, Park Namgyeong, Hwang Deok-Sang, Park Seon-Young, Kim Soyoung, Bae Hyunsu

机构信息

Department of Physiology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.

Department of Clinical Korean Medicine, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul 02447, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Dec 21;25(24):13682. doi: 10.3390/ijms252413682.

DOI:10.3390/ijms252413682

PMID:39769442

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11727661/

Abstract

CX3CR1-transduced regulatory T cells (Tregs) have shown potential in reducing neuroinflammation by targeting microglial activation. Reactive microglia are implicated in neurological disorders, and CX3CR1-CX3CL1 signaling modulates microglial activity. The ability of CX3CR1-transduced Tregs to inhibit LPS-induced neuroinflammation was assessed in animal models. CX3CR1 Tregs were administered to LPS-induced and 3xTg Alzheimer's mouse models, resulting in reduced proinflammatory marker expression in both the cortices and hippocampi. In the 3xTg Alzheimer's model, neuroinflammation was significantly reduced, demonstrating the efficacy of CX3CR1 Tregs even in chronic neuroinflammatory conditions. These findings highlight the therapeutic potential of CX3CR1 Treg therapy in modulating microglial activity and offer promising treatment strategies for neurodegenerative diseases.

摘要

CX3CR1转导的调节性T细胞（Tregs）已显示出通过靶向小胶质细胞激活来减轻神经炎症的潜力。反应性小胶质细胞与神经疾病有关，并且CX3CR1-CX3CL1信号传导调节小胶质细胞活性。在动物模型中评估了CX3CR1转导的Tregs抑制脂多糖（LPS）诱导的神经炎症的能力。将CX3CR1 Tregs给予LPS诱导的和3xTg阿尔茨海默病小鼠模型，导致皮质和海马中促炎标志物表达降低。在3xTg阿尔茨海默病模型中，神经炎症显著减轻，表明即使在慢性神经炎症条件下CX3CR1 Tregs也有效。这些发现突出了CX3CR1 Treg疗法在调节小胶质细胞活性方面的治疗潜力，并为神经退行性疾病提供了有前景的治疗策略。