Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD4- CD8+ cytotoxic T-cells and under some circumstances there is a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient, providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds.
The B2mtm1Unc allele was generated in the laboratory of Dr. Beverly Koller and Dr. Oliver Smithies at The University of North Carolina at Chapel Hill. This targeted disruption used the 129P2/OlaHsd derived E14TG2a ES cell line. The C3H/HeJ strain was produced in the laboratory of Dr. Derry Roopenian at The Jackson Laboratory by backcrossing the B2mtm1Unc allele from a segregating 129;B6 background 13 times to C3H/HeJ inbred mice.
|Allele Name||targeted mutation 1, University of North Carolina|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||b2mnull; beta2M-; beta2m0; beta2mnull; beta2mo; beta2mtm1Unc; beta2MKO; beta2-m-KO; I0; MHC-I-|
|Gene Symbol and Name||B2m, beta-2 microglobulin|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||Insertion of a neomycin-resistance gene into the second exon.|
|Mutations Made By|| |
Dr. Oliver Smithies, University of North Carolina at Chapel Hill