The CD24-Siglec G axis protects mice against cuprizone-induced oligodendrocyte loss: targeting danger signal for neuroprotection  

作　　者：Ning Li Pan Zheng Yang Liu 

机构地区：[1]Center for Cancer and Immunology Research,Children’s Research Institute,Children’s National Health System,Washington,20010,DC,USA

出　　处：《Cellular & Molecular Immunology》2018年第1期79-81,共3页中国免疫学杂志（英文版）

摘　　要：Oligodendrocytes play a critical role in neuroprotection by both remyelination-dependent and remyelination-independent mechanisms and confer protection in both inflammatory and degenerative diseases that involve the central nervous system,including multiple sclerosis,Alzheimer’s disease and potentially Parkinson’s disease.1,2,3,4 Although accumulating data have supported a major role for inflammation in the susceptibility of oligodendrocytes to cuprizone,the molecular pathways that regulate oligodendrocyte survival have not been well established.Here,we report that the targeted mutation of either Cd24 or Siglecg,which forms an axis that selectively regulates the innate inflammatory response to danger-associated molecular patterns(DAMPs),protects mice against cuprizone-induced oligodendrocyte loss.Moreover,the systemic administration of CD24Fc,which is known to stimulate Siglec G signaling and suppress the inflammatory response in vivo,protects oligodendrocytes against chronic exposure to cuprizone.Our data suggest that the host response to cellular injury actively participates in oligodendrocyte loss and provides a new approach to maintain oligodendrocytes under pathological conditions.

关 键 词：CD24 CUPRIZONE inflammation 

分 类 号：R73[医药卫生—肿瘤]