小胶质细胞
谱系(遗传)
巨噬细胞
实验性自身免疫性脑脊髓炎
表型
生物
受体
细胞生物学
神经科学
免疫学
医学
中枢神经系统
基因
遗传学
炎症
体外
作者
Robert M. Hoek,Sigrid R. Ruuls,Craig A. Murphy,Gavin J. Wright,Ruth S. Goddard,Sandra Zurawski,Bianca Blom,Margit Homola,Wolfgang J. Streit,Marion H. Brown,A. Neil Barclay,Jonathon D. Sedgwick
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2000-12-01
卷期号:290 (5497): 1768-1771
被引量:995
标识
DOI:10.1126/science.290.5497.1768
摘要
OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.
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