CX3CR1型
生物
小胶质细胞
CX3CL1型
细胞生物学
趋化因子受体
报告基因
绿色荧光蛋白
转染
受体
基因靶向
免疫学
趋化因子
基因
免疫系统
基因表达
炎症
遗传学
作者
Steffen Jung,Júlio Aliberti,Petra Graemmel,Mary Jean Sunshine,Georg W. Kreutzberg,Alan Sher,Dan R. Littman
标识
DOI:10.1128/mcb.20.11.4106-4114.2000
摘要
The seven-transmembrane receptor CX3CR1 is a specific receptor for the novel CX3C chemokine fractalkine (FKN) (neurotactin). In vitro data suggest that membrane anchoring of FKN, and the existence of a shed, soluble FKN isoform allow for both adhesive and chemoattractive properties. Expression on activated endothelium and neurons defines FKN as a potential target for therapeutic intervention in inflammatory conditions, particularly central nervous system diseases. To investigate the physiological function of CX3CR1-FKN interactions, we generated a mouse strain in which the CX3CR1 gene was replaced by a green fluorescent protein (GFP) reporter gene. In addition to the creation of a mutant CX3CR1 locus, this approach enabled us to assign murine CX3CR1 expression to monocytes, subsets of NK and dendritic cells, and the brain microglia. Analysis of CX3CR1-deficient mice indicates that CX3CR1 is the only murine FKN receptor. Yet, defying anticipated FKN functions, absence of CX3CR1 interferes neither with monocyte extravasation in a peritonitis model nor with DC migration and differentiation in response to microbial antigens or contact sensitizers. Furthermore, a prominent response of CX3CR1-deficient microglia to peripheral nerve injury indicates unimpaired neuronal-glial cross talk in the absence of CX3CR1.
科研通智能强力驱动
Strongly Powered by AbleSci AI