Asking one mechanism in glial cells during neuroinflammation
Xiaoli Guo
Chikako Harada
Takayuki Harada
Visual Research Project,Tokyo Metropolitan Institute of Medical Science,Tokyo,Japan
摘要：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).
机标关键词：mechanismcellsaskingduringeuroglialinflammation
论文发表日期：2025-04-27
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1077-1078 )