These NOD-scid.RIPB7 mice express a transgene encoding the human CD80 T cell co-stimulatory molecule.
Dr. David Serreze, The Jackson Laboratory
Genetic Background | Generation |
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|
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Spontaneous | Prkdc | protein kinase, DNA activated, catalytic polypeptide |
Allele Type |
---|
Transgenic (Inserted expressed sequence, Humanized sequence) |
These mice are characterized by pancreatic beta cells that express a rat insulin promoter (Rip) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. They are an excellent source of MHC class I positive, CD80 transgene-expressing islet cells, a potent antigenic reagent for propagating diabetogenic CD8+ T lymphocytes derived from NOD mice in vitro. The presence of the Prkdcscid allele eliminates the possibility that isolated islet cells will introduce contaminating T lymphocytes onto cultures.
Mice homozygous for the Prkdcscid mutation and hemizygous for the Tg(Ins2-CD80)3B7Flv transgene are viable and fertile. In 2016, it is the experience of The Jackson Laboratory Repository that bi-weekly treatment of medicated water (described below) greatly improves colony health / is required for colony to thrive.
NOD mice homozygous for the Prkdcscid mutation are characterized by an absence of functional T cells and B cells - resulting in severe immunodeficiency.
As such, and similar to other immunodeficient strains, maintenance in high health status (specific pathogen-free) vivaria promotes overall colony health. If mice homozygous for Prkdcscid are maintained in low health barrier rooms, the use of medicated water (e.g., sulfatrim/trimethoprim-sulfa or enrofloxacin/Baytril) is suggested to increase overall colony health.
A transgenic construct containing the human CD80 gene driven by the rat insulin promoter 1 (Rip) was injected fertilized eggs of a mating between C57BL/6 and CBA/Ca strains in the laboratory of Dr. Richard Flavell (Yale University). Founder animals were obtained and bred to C57BL/6 mice, and partially transferred to the NOD background through five backcross generations. Mice with the partial NOD background were obtained from the Flavell laboratory and crossed to NOD.CB-17-Prkdcscid/J (Jax strain 001303) for eight backcross generations by Dr. David Serreze, The Jackson Laboratory. Marker assistance was employed in backcrossing protocol.
Expressed Gene | CD80, CD80 molecule, human |
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Site of Expression |
Allele Name | severe combined immunodeficiency |
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Allele Type | Spontaneous |
Allele Synonym(s) | SCID |
Gene Symbol and Name | Prkdc, protein kinase, DNA activated, catalytic polypeptide |
Gene Synonym(s) | |
Site of Expression | T and B lymphocytes. |
Strain of Origin | C.BKa-Ighb/Icr |
Chromosome | 16 |
Molecular Note | A T-to-A transversion point mutation at a position corresponding to codon 4046 (codon 4095 in transcript ENSMUST00000023352.8) created a premature stop codon (p.Y4046*). |
Allele Name | transgene insertion 3B7, Richard Flavell |
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Allele Type | Transgenic (Inserted expressed sequence, Humanized sequence) |
Allele Synonym(s) | RIP-B7; RIP-B7.1; RIP-B7-1; RIP-CD80 |
Gene Symbol and Name | Tg(Ins2-CD80)3B7Flv, transgene insertion 3B7, Richard Flavell |
Gene Synonym(s) | |
Promoter | Ins2, insulin 2, rat |
Expressed Gene | CD80, CD80 molecule, human |
Strain of Origin | (C57BL/6 x CBA/Ca)F2 |
Chromosome | UN |
General Note | Mice carrying this transgene that also are homozygous for Prkdcscid are characterized by pancreatic beta cells that express a rat insulin II promoter regulated transgene encoding the human CD80 T cell co-stimulatory molecule. |
Molecular Note | The transgene contains a human CD80 antigen gene driven by the rat insulin II promoter (Ins2). |
Mutations Made By | Dr. Richard Flavell, Yale University School of Medicine |
Mice homozygous for the Prkdcscid mutation and hemizygous for the Tg(Ins2-CD80)3B7Flv transgene are viable and fertile. As of 2016, it is the experience of The Jackson Laboratory Repository that bi-weekly treatment of medicated water (described below) greatly improves colony health and is required for colony to thrive.
NOD mice homozygous for the Prkdcscid mutation are characterized by an absence of functional T cells and B cells - resulting in severe immunodeficiency. As such, and similar to other immunodeficient strains, maintenance in high health status (specific pathogen-free) vivaria promotes overall colony health. If mice homozygous for Prkdcscid are maintained in low health barrier rooms, the use of medicated water (e.g., sulfatrim/trimethoprim-sulfa or enrofloxacin/Baytril) is suggested to increase overall colony health.
The Jackson Laboratory mating system - Prkdcscid/ Prkdcscid, Tg/? XPrkdcscid/Prkdcscid, Tg/?
Genotypes available - Prkdcscid/Prkdcscid, Tg/? and Prkdcscid/Prkdcscid, +/+
Affected mutant - Prkdcscid/ Prkdcscid/, Tg/?
Breeder pairs-Prkdcscid/ Prkdcscid/, Tg/? x Prkdcscid/ Prkdcscid/, Tg/?
When using the NOD-scid.RIPB7 mouse strain in a publication, please cite the originating article(s) and include JAX stock #004346 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Homozygous for Prkdc<scid>,Homozygous or Hemizygous or Non carrier for Tg(Ins2-CD80)3B7Flv |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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