CX3CR1 is the receptor for chemokine fractalkine (CX3CL1) and is expressed in monocytes, T cells, NK cells, as well as neurons, microglia cells, and astrocytes. Fractalkine mediates adhesion and chemotaxis of the cells expressing CX3CR1. An initial analysis indicates that Cx3cr1-/- mice on an atherogenic ApoE-/- background have reduced susceptibility to atherosclerosis.
Origin: Drs. Christopher Combadiere, Ji-Liang Gao and Philip Murphy in the Laboratory of Host Defenses, NIAID, made the Cx3cr1-/- mouse by targeted gene disruption in 1998. The Cx3cr1 gene was mutated by replacing a 0.6kb DNA fragment containing the Cx3cr1 start codon with a neomycin resistance gene. The disrupted gene was introduced to 129/Sv ES cells to create chimeric mice, and then the chimeric founders were backcrossed to C57BL/6NAi mice for 10 generations in the NIAID barrier facility at Taconic. At this point, it was discovered that the C57BL/6NAi line had become contaminated with the IFNγ knockout gene. Line 167 was then backcrossed to C57BL/6NTac (Taconic B6) for 5 generations in order to eliminate the contaminating gene and put the strain onto the Taconic C57BL/6 subline background.
Initial Publication: Combadiere C, Potteaux S, Gao JL, Esposito B, Casanova S, Lee EJ, Debre P, Tedgui A, Murphy PM, Mallat Z. Decreased atherosclerotic lesion formation in CX3CR1/apolipoprotein E double knockout mice. Circulation. 2003; 107(7): 1009-16.