Asking one mechanism in glial cells during neuroinflammation  

作　　者：Xiaoli Guo Chikako Harada Takayuki Harada 

机构地区：[1]Visual Research Project,Tokyo Metropolitan Institute of Medical Science,Tokyo,Japan

出　　处：《Neural Regeneration Research》2025年第4期1077-1078,共2页中国神经再生研究（英文版）

基　　金：supported by Japan Society for the Promotion of Science(JSPS)KAKENHI Grants-in-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：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).

关 键 词：INFLAMMATION CLINICAL 

分 类 号：R744.51[医药卫生—神经病学与精神病学]