JAX Mouse Strain Datasheet - 002309

NOD.129P2(B6)-B2m^tm1Unc/J

Stock No:: 002309 |; NOD β₂m KO

Cryo Recovery

Overview

Also Known As: NOD β₂m KO

These B2m knock-out mice exhibit little if any MHC class I protein expression on the cell surface with deficiency in CD8⁺ cytotoxic T-cells, NK1⁺ T cells, and decreased levels of serum Ig.

Donating Investigator

Dr. Derry Roopenian, The Jackson Laboratory

Genetic overview

Genetic Background	Generation
001289 NOD/ShiLt

B2m^tm1Unc

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	B2m	beta-2 microglobulin

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Research Applications

Diabetes and Obesity Research
Hematological Research
Immunology, Inflammation and Autoimmunity Research
Internal/Organ Research
Metabolism Research
Research Tools

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances 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. Other traits of B2M deficient mice include: NK cell deficiency, NK1⁺ T cells deficiency and decreased levels of serum Ig. Some forms of lupus autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). The B2m^tm1Un mutation backcrossed to the NOD/Lt strain serves as a MHC class I-negative, CD8⁺ deficient diabetes resistant stock for comparison to the NOD/LtJ strain (Stock No. 001976). The elimination of cell surface MHC class I expression blocks both insulitis and autoimmune diabetes in NOD/Lt mice. A disadvantage of this strain is that CD4⁺ T cells are not tolerant to MHC class I positive syngeneic cells. These mice provide an excellent source for insulitis-free, MHC class I-bare NOD islets for transplantation studies.

Development

The B2m^tm1Unc mutant strain was developed in the laboratory of Dr. Beverly Koller and Dr. Oliver Smithies at the University of North Carolina at Chapel Hill. It was generated by a targeted disruption of the B2m gene. The 129-derived E14TG2a ES cell line was used. The NOD/LtJ strain was produced in the laboratory of Dr. Derry Roopenian at The Jackson Laboratory by backcrossing the B2m^tm1Unc mutation 10 times to NOD/LtJ inbred mice.

Control Suggestions

Additional control strains are available depending on the researchers needs.
001976 NOD/ShiLtJ

Additional Information

Considerations for Choosing Controls

Selected References

Koller BH; Marrack P; Kappler JW; Smithies O. 1990. Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells. Science 248(4960):1227-30. PubMed: 2112266 MGI: J:64451

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Genetics

B2m^tm1Unc

Allele Symbol: B2m^tm1Unc

Allele Name	targeted mutation 1, University of North Carolina
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	I⁰; MHC-I^-; b2m^null; beta2-m-KO; beta2M-; beta2MKO; beta2m⁰; beta2m^null; beta2m^o; beta2m^tm1Unc
Gene Symbol and Name	B2m, beta-2 microglobulin
Gene Synonym(s)	IMD43; Ly-m11; Ly-m11; beta 2 microglobulin; beta2-m; lymphocyte antigen m11
Strain of Origin	129P2/OlaHsd
Chromosome	2
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

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
- Islet Transplantation Studies
- Type 1 Diabetes (IDDM) Analysis Strains
  - NOD Congenics with Mutations Affecting Immunocompetence

Genotype: B2m^tm1Unc related

Hematological Research
- Anemia, Iron Deficiency and Transport Defects
  - hemochromatosis
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - MHC class I deficiency
Internal/Organ Research
- Liver Defects
  - hemochromatosis
Metabolism Research
- Hemochromatosis
  - iron metabolism defects
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - MHC class I deficiency

Mammalian Phenotype Terms by Genotype

Genotype: B2m^tm1Unc/B2m^tm1Unc
NOD.129P2-B2m^tm1Unc

endocrine/exocrine gland phenotype

abnormal pancreatic beta cell morphology
- homozygous-null NOD mice show almost no insulitis and still possess normal beta cells; control NOD mice show insulitis and a high degree of beta cell destruction

immune system phenotype

absent CD8-positive, alpha-beta T cells
- mice lack CD8+ T cells

decreased susceptibility to autoimmune diabetes
- females remain disease-free compared
- no homozygous mice become diabetic by 4 months of age, while over 70% of control NOD mice become diabetic (blood glucose >16.7 mM; positive urine glucose test) by 4 months of age

hematopoietic system phenotype

absent CD8-positive, alpha-beta T cells
- mice lack CD8+ T cells

References

Koller BH; Marrack P; Kappler JW; Smithies O. 1990. Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells. Science 248(4960):1227-30. PubMed: 2112266 MGI: J:64451

Additional References

Serreze DV; Leiter EH; Christianson GJ; Greiner D; Roopenian DC. 1994. Major histocompatibility complex class I-deficient NOD-B2mnull mice are diabetes and insulitis resistant. Diabetes 43(3):505-9. PubMed: 8314025 MGI: J:17000
Sproule TJ; Jazwinska EC; Britton RS; Bacon BR; Fleming RE; Sly WS; Roopenian DC. 2001. Naturally variant autosomal and sex-linked loci determine the severity of iron overload in beta 2-microglobulin-deficient mice. Proc Natl Acad Sci U S A 98(9):5170-4. PubMed: 11309500 MGI: J:68985
Wicker LS; Leiter EH; Todd JA; Renjilian RJ; Peterson E; Fischer PA; Podolin PL; Zijlstra M; Jaenisch R; Peterson LB. 1994. Beta 2-microglobulin-deficient NOD mice do not develop insulitis or diabetes. Diabetes 43(3):500-4. PubMed: 8314024 MGI: J:16999

Additional - B2m^tm1Unc related

Adoro S; Erman B; Sarafova SD; Van Laethem F; Park JH; Feigenbaum L; Singer A. 2008. Targeting CD4 coreceptor expression to postselection thymocytes reveals that CD4/CD8 lineage choice is neither error-prone nor stochastic. J Immunol 181(10):6975-83. PubMed: 18981117 MGI: J:140942
Adoro S; McCaughtry T; Erman B; Alag A; Van Laethem F; Park JH; Tai X; Kimura M; Wang L; Grinberg A; Kubo M; Bosselut R; Love P; Singer A. 2011. Coreceptor gene imprinting governs thymocyte lineage fate. EMBO J 31(2):366-77. PubMed: 22036949 MGI: J:180236
Adoro S; Park KH; Bettigole SE; Lis R; Shin HR; Seo H; Kim JH; Knobeloch KP; Shim JH; Glimcher LH. 2017. Post-translational control of T cell development by the ESCRT protein CHMP5. Nat Immunol 18(7):780-790. PubMed: 28553951 MGI: J:258169
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