-
Contains a disruption of the beta-2-microglobulin gene
-
Deficient in MHC Class I molecule expression
-
Exhibits depletion of CD8+ T cells
-
Lack the NK1.1+ CD4+ T-cell population as well, because of dependence on MHC Class 1b molecule CD1 for development
-
Useful in transplantation, gene therapy, and immunological disease research
Genetic Background:
C57BL/6 Background Origin:
The B2m mouse was developed in the laboratory of Rudolf Jaenisch at the Whitehead Institute. The model was created by targeting the B2m gene in D3 ES cells and injecting the targeted cells into C57BL/6J blastocysts. Resultant chimeras were backcrossed to C57BL/6 for five generations (N5). GenPharm International received stock from the Jaenisch lab in 1991. Taconic received stock in February 1994. The mice were then backcrossed seven generations (N12) to C57BL/6NTac and derived by embryo transfer. Heterozygotes were intercrossed to homozygosity. The colony was maintained through incrossing of homozygotes. Genetics:
Wild type for Nnt mutation Color:
Black Species:
Mouse Initial Publication:
Zijlstra M, Bix M, Simister NE, Loring JM, Raulet DH, Jaenisch R. (1990)
β2-Microglobulin deficient mice lack CD4-8+ cytolytic T cells,
Nature, 344(6268):742-746.