癫痫发作中Th17/Treg细胞失衡的研究进展

IF 4.2 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-06-13 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S524814
Liu Mu, Yan Rong, Yang Jia Xin, Hong Zhang, Zucai Xu
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引用次数: 0

摘要

由于大脑中异常的神经元放电,癫痫与广泛的神经系统疾病有关,这对患者的生活质量产生重大不利影响,并增加其死亡风险。免疫失衡,特别是Th17/Treg细胞平衡的破坏,随着我们对神经免疫相互作用的理解的提高,在癫痫的病理生理学中得到了越来越多的关注。本文探讨了其潜在的治疗作用,并深入讨论了Th17/Treg细胞失衡导致癫痫发展的过程。主要的重点是这种不平衡损害血脑屏障完整性、神经炎症和其他因素的机制。在治疗方面,通过生酮饮食、纳米材料和基因编辑等方法,靶向Th17/Treg轴进行免疫调节,显示出恢复免疫平衡的良好前景。通过进一步了解Th17/Treg细胞失衡与癫痫病因之间的联系,这项工作为创造创新的免疫治疗方法提供了重要的理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Research Progress on Th17/Treg Cell Imbalance in Epileptic Seizures.

Epilepsy is associated with widespread neurological circumstances due to aberrant neuronal discharges in the brain, which have significant adverse effects on patient's quality of life and increase their risk of death. Immune imbalance, particularly disruption of the Th17/Treg cell balance, has gained increasing attention in the pathophysiology of epilepsy as our understanding of neuroimmune interactions improves. This paper examines the potential therapeutic effects and thoroughly discusses the processes by which the Th17/Treg cell imbalance contributes to the development of epilepsy. The primary emphasis is on the mechanism by which this imbalance impairs blood-brain barrier integrity, neuroinflammation, and other elements. On the therapeutic front, targeting the Th17/Treg axis for immune regulation-through approaches such as ketogenic diets, nanomaterials, and gene editing-shows promising prospects for restoring immune balance. By furthering our knowledge of the connection between Th17/Treg cell imbalance and epilepsy etiology, this work offers a crucial theoretical foundation for creating innovative immunotherapy approaches.

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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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