NOD.129S2(B6)-H2-Ab1^b-tm1Doi/DvsJ

Stock number: 004256
Product name: MHC class II-deficient
Research areas: Diabetes and Obesity Research, Research Tools

Detailed description

NOD/Lt females homozygous for this class II targeted disruption are protected from autoimmune diabetes but develop pancreatitis. They lack peripheral CD4⁺ T cells but have mature peripheral B cells.

Development

The H2-Ab1 knock-out allele in Stock No. 004256 was originally reported to be H2-Ab1^b-tm1Gru (created by Dr. Michael J. Grusby; while at Harvard) - harboring a forward-oriented neomycin resistance cassette that disrupts H2-Ab1 exon 2 (and made in ES cells with a deletion in the promoter region of H2-Ea). In 2018, quality control efforts at The Jackson Laboratory were completed that revealed Stock No. 004256 instead has the very similar H2-Ab1^tm1Doi knock-out allele (created by Drs. Christophe Benoist and Diane Mathis; while at INSERM) - harboring a reverse-oriented neomycin resistance cassette that disrupts H2-Ab1 exon 2 (and made in ES cells with a deletion in the promoter region of H2-Ea). The Ab^o knock-out allele is on chromosome 17.

Allele

Symbol: H2-Ab1^b-tm1Doi
Name: targeted mutation 1, Christophe Benoist and Diane Mathis
MGI accession ID: MGI:1927483
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: A beta⁰; A^bbeta^-; AB0; Abeta-; Class II⁰; H2-Ab1^tm1Dim; H2-Ab1^tm1Doi; H2-Ab1tm1Doi; II⁰; MHC class II-; MHCII^-; MHC-II-k.o.
Marker symbol: H2-Ab1
Marker name: histocompatibility 2, class II antigen A, beta 1
Marker synonyms: A beta; Abeta; Bb; CELIAC1; DQB2; H-2Ab; H2-Ab; HLA-DQB; HLA-DQB1; HLA-DXB; I-A^b; Ia2; Ia-2; IAb; I-Abeta; IDDM1; Rmcs1; RT1.B
Chromosome: 17
Strain of origin: 129S2/SvPas
Molecular note: The second exon was disrupted by the insertion of a neomycin resistance gene. In addition, the ES cell line used was derived from the 129S2/SvPas strain, which carries a deletion in the promoter region of H2-Ea. Consequently, these MHC class II molecule-deficient mice lacked cell surface expression of both class II-A and class II-E MHC proteins.