遗传 ›› 2022, Vol. 44 ›› Issue (4): 289-299.doi: 10.16288/j.yczz.22-030

• 综述 • 上一篇    下一篇

致病性Th17细胞在神经炎症中的作用及调控机制的研究进展

戴鸿宇1,2(), 季东1,2, 谈程1,2, 孙杰3(), 姚昊1,2()   

  1. 1. 南京医科大学第二附属医院心血管中心,南京 210003
    2. 南京医科大学第二附属医院麻醉科,南京 210011
    3. 东南大学附属中大医院麻醉科,南京 210009
  • 收稿日期:2022-02-12 修回日期:2022-03-18 出版日期:2022-04-20 发布日期:2022-03-25
  • 通讯作者: 孙杰,姚昊 E-mail:daihongyu@njmu.edu.cn;dgsunjie@hotmail.com;yaohao@njmu.edu.cn
  • 作者简介:戴鸿宇,在读硕士研究生,专业方向:麻醉学。E-mail: daihongyu@njmu.edu.cn
  • 基金资助:
    江苏省科技厅省级重点研发计划(社会发展)项目编号(SBE2021741263);南京医科大学第二附属医院789人才培养计划资助编号(789ZYRC080236)

Research progress on the role and regulatory mechanism of pathogenic Th17 cells in neuroinflammation

Hongyu Dai1,2(), Dong Ji1,2, Cheng Tan1,2, Jie Sun3(), Hao Yao1,2()   

  1. 1. Department of Cardiovascular Surgery Center, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210003, China
    2. Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China
    3. Department of Anesthesiology, Zhongda Hospital, Medical School, Southeast University, Nanjing 210009, China
  • Received:2022-02-12 Revised:2022-03-18 Online:2022-04-20 Published:2022-03-25
  • Contact: Sun Jie,Yao Hao E-mail:daihongyu@njmu.edu.cn;dgsunjie@hotmail.com;yaohao@njmu.edu.cn
  • Supported by:
    Supported by the Provincial Key R&D Program (Social Development) of Science and Technology Department of Jiangsu Province No(SBE2021741263);the 789 Talents Training Program of the Second Affiliated Hospital of Nanjing Medical University No(789ZYRC080236)

摘要:

神经炎症是中枢神经系统在损伤、感染、毒素等各种影响内稳态因素的刺激下产生的复杂免疫反应,涉及驻留在中枢神经系统中的多种免疫细胞。持续存在的神经炎症是所有神经系统疾病(包括神经发育、神经退行性和精神性疾病)病因和病程的共同特性。Th17细胞是CD4+T细胞的一个重要亚型,在稳态条件下介导对细胞外细菌和真菌的免疫反应,维持肠道粘膜屏障的防御功能。但当体内细胞因子微环境发生炎症性改变时,Th17细胞可以转化为具有高度促炎性的致病表型,在炎症性疾病的发生发展中起着至关重要的作用。本文主要对致病性Th17细胞的分化调控及其在神经炎症中的作用进行了系统综述,对于理解免疫系统和神经系统之间的相互作用具有一定参考意义。

关键词: 神经炎症, 致病性Th17细胞, 血脑屏障, RORγt;

Abstract:

Neuroinflammation is a complex immune response in the central nervous system against various factors such as injury, infection and toxins which interfere with homeostasis, involving a variety of immune cells lingering in the central nervous system. Persistent neuroinflammation is a common denominator of the etiology and course of all neurological diseases, including neurodevelopmental, neurodegenerative and psychiatric disorders, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and depression. Th17 cells, known as an important subtpye of CD4+ T cells, mediate immune responses against extracellular bacteria and fungi in steady-state and maintain the defense function of the intestinal mucosal barrier. However, when the cytokine microenvironment in vivo undergoes inflammatory changes, Th17 cells can transform into a highly pro-inflammatory pathogenic phenotype, break through the blood-brain barrier and recruit more inflammatory cells to participate in neuroinflammation, ultimately leading to neurodegeneration. In this review, we summarize the differentiation regulation of pathogenic Th17 cells and their roles in neuroinflammation, which is informative for understanding the interactions between immune system and nervous system.

Key words: neuroinflammation, pathogenic Th17 cells, blood-brain barrier, RORγt;