Homozygous mice are viable but fail to thrive (few pups are produced). Maintaining homozygous mice in a gnotobiotic vivarium may enhance strain breeding performance. Heterozygous mice are viable and fertile with no reported needs for special husbandry. The donating investigator reports that Cxcr2-deficient mice on the SJL/J genetic background are resistant to experimental autoimmune encephalomyelitis (EAE) protocols compared to susceptible SJL/J wildtype mice. Cxcr2-deficiency on other genetic backgrounds is associated with several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. In addition, homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studying inflammation, immunology, cancer biology, demyelinating autoimmune disease (such as multiple sclerosis and EAE protocols), and myelin repair.

There are reported differences for Cxcr2-deficient mice on different genetic backgrounds. On a C57BL/6 genetic background, Cxcr2-deficiency imparts resistance to cuprizone-induced demyelination compared to wildtype C57BL/6 mice. Only modest demyelination is observed independent of Cxcr2-deficiency on the cuprizone-resistant BALB/c genetic background. Similarly, BALB/c inbred mice are relatively resistant to experimental autoimmune encephalomyelitis (EAE), while Cxcr2-deficiency on EAE-susceptible C57BL/6 or (SWRxSJL)F1 genetic backgrounds result in decreased incidence, decreased mortality, and enhanced recovery. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Mice harboring this chemokine (C-X-C motif) receptor 2 (Cxcr2) "knockout" mutation may be useful in studying inflammation, immunology, cancer biology, demyelinating autoimmune disease (such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) protocols), and myelin repair.

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