C57BL/6-Cd200tm1Jods/H
| Status | Available to order |
| EMMA ID | EM:13041 |
| International strain name | C57BL/6-Cd200tm1Jods/H |
| Alternative name | C57BL/6-Cd200tm1Jods |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Cd200tm1Jods, |
| Gene/Transgene symbol | Cd200 |
Information from provider
| Provider | Andrew Dick |
| Provider affiliation | Translational Health Sciences, Ophthalmology, University of Bristol |
| Genetic information | Cd200 knock-out mouse line. A portion of exon 3 was replaced by a neomycin selection cassette (see http://www.informatics.jax.org/allele/MGI:2429651). |
| Phenotypic information | Homozygous:Cd200 homozygous (-/-) knock-out mice appear normal, breed normally and exhibit a normal life-span with no obvious behavioural differences. Cd200 is a broadly expressed membrane glycoprotein, important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and are increased in number. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 results in a more rapid onset of experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune uveoretinitis (EAU). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Heterozygous:Cd200 heterozygous (+/-) knock-out mice appear normal, breed normally and exhibit a normal lifespan with no obvious behavioural differences. |
| Breeding history | >50 |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | yes |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Literature references
- Down-regulation of the macrophage lineage through interaction with OX2 (CD200).;Hoek R M, Ruuls S R, Murphy C A, Wright G J, Goddard R, Zurawski S M, Blom B, Homola M E, Streit W J, Brown M H, Barclay A N, Sedgwick J D, ;2000;Science (New York, N.Y.);290;1768-71; 11099416