中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (4): 1077-1078.doi: 10.4103/NRR.NRR-D-24-00225

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

询问神经炎症过程中神经胶质细胞的一种机制

  

  • 出版日期:2025-04-15 发布日期:2024-06-30

Asking one mechanism in glial cells during neuroinflammation

Xiaoli Guo* , Chikako Harada, Takayuki Harada   

  1. Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
  • Online:2025-04-15 Published:2024-06-30
  • Contact: Xiaoli Guo, PhD, guo-xl@igakuken.or.jp.
  • Supported by:
    This work was supported by Japan Society for the Promotion of Science (JSPS) KAKENHI Grantsin-Aid for Scientific Research (JP21K09688 and JP24K12795 to XG; JP22K09804 to CH; JP19KK0229, JP21H02819, JP21K18279, and JP24H00583 to TH), Shiseido Female Researcher Science Grant (to XG) and the Takeda Science Foundation (to TH).

摘要: https://orcid.org/0000-0002-4835-5690 (Xiaoli Guo)

Abstract: Multiple sclerosis (MS), which is characterized by inflammatory demyelination in the central nervous system (CNS), is the most common neurological disease in the young adult population. Experimental autoimmune encephalomyelitis (EAE), an animal model of MS, is often used in preclinical studies. Accumulating data indicate that in addition to immune cells such as T cells and dendritic cells, CNS resident microglia and astrocytes play important roles in demyelinating neuroinflammation (Healy et al., 2022). In particular, microglia are key immune-competent cells that can respond to environmental changes. Conditional depletion of transforming growth factor-β-activated kinase 1, a mitogen-associated protein kinase kinase kinase, in microglia is reported to reduce CNS inflammation and diminish axonal and myelin damage significantly. This suggests that elucidating the mechanisms of microglia-specific responses during pathologies may help in the development of treatments that reduce EAE/MS disease severity (Goldmann et al., 2013).