Analysis of Fractalkine Receptor CX3CR1 Function by Targeted Deletion and Green Fluorescent Protein Reporter Gene Insertion

• DOI: 10.1128/mcb.20.11.4106-4114.2000
• Publication Date: 2002-07-27T10:03:40Z
• Authors: Steffen Jung; Julio Aliberti; Petra Graemmel; Mary Jean Sunshine; Georg W. Kreutzberg; Alan Sher; Dan R. Littman
• Keywords: CX3CR1; CX3CL1; Gene targeting

The seven-transmembrane receptor CX3CR1 is a specific for the novel CX3C chemokine fractalkine (FKN) (neurotactin). In vitro data suggest that membrane anchoring of FKN, and existence shed, soluble FKN isoform allow both adhesive chemoattractive properties. Expression on activated endothelium neurons defines as potential target therapeutic intervention in inflammatory conditions, particularly central nervous system diseases. To investigate physiological function CX3CR1-FKN interactions, we generated mouse strain which gene was replaced by green fluorescent protein (GFP) reporter gene. addition to creation mutant locus, this approach enabled us assign murine expression monocytes, subsets NK dendritic cells, brain microglia. Analysis CX3CR1-deficient mice indicates only receptor. Yet, defying anticipated functions, absence interferes neither with monocyte extravasation peritonitis model nor DC migration differentiation response microbial antigens or contact sensitizers. Furthermore, prominent microglia peripheral nerve injury unimpaired neuronal-glial cross talk CX3CR1.