JAX Mouse Strain Datasheet - 003903

NOD.129S2-Ighm^tm1Cgn/Dvs

Stock No:: 003903

Availability Varies

Overview

NOD mice homozygous for the Ighm^tm1Cgn allele do not express membrane-bound IgM, lack mature B-cells, are free of insulitis, and do not develop IDDM.

Genetic overview

Genetic Background	Generation
NOD	N11F15 (29-AUG-16)

Ighm^tm1Cgn

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ighm	immunoglobulin heavy constant mu

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Research Applications

Immunology, Inflammation and Autoimmunity Research
Research Tools

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Detailed Description

NOD mice homozygous for the Ighm^tm1Cgn allele do not express membrane-bound IgM. Ighm deficient mice lack mature B-cells, although some B-cells may be produced using a C gene other than mu. These mice are virtually free of insulitis: at most, presence of only perivascular/periductal leukocytes is detected. No intra-islet infiltrates are found. Results indicate that insulin dependent diabetes mellitus (IDDM) is not delayed, but prevented because of a lack of B cell autoreactive T cell responses. Therefore, the elimination of B lymphocytes by congenic transfer of the Ighm^tm1Cgn mutation is sufficient to block IDDM development in an otherwise susceptible NOD mouse strain. (Kitamura 1991, Serreze 1996)

Development

The Ighm gene was disrupted by insertion of a translational stop codon and neomycin-resistence gene close to the 5' boundary of the first exon. The disrupted gene was transfected into D3 ES cells (derived from 129S2/SvPas). Male founders were bred and maintained on a C57BL/6 prior to backcross onto NOD/Lt for more than 10 generations. The Ighm^tm1Cgn allele is maintained homozygous by brother-sister mating. (Kitamura 1991)

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Selected References

Serreze DV; Chapman HD; Varnum DS; Hanson MS; Reifsnyder PC; Richard SD; Fleming SA; Leiter EH; Shultz LD. 1996. B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: analysis of a new speed congenic stock of NOD.Ig mu null mice. J Exp Med 184(5):2049-53. PubMed: 8920894 MGI: J:37287

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Genetics

Ighm^tm1Cgn

Allele Symbol: Ighm^tm1Cgn

Allele Name	targeted mutation 1, University of Cologne
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	B cell^-; BCKO; BCR-; BKO; Cmu ^-; Ig- muMT; Ig^-; IgH-; IgH^muMT; Igh-6-; Igh-6^null; Igh-6^tm1Cgn; Igh-6tm1CgnmuMT⁰; Ighm^-; Igmu^null; mu-MT^-; muIgKO; muMT; muMt-; mum^-
Gene Symbol and Name	Ighm, immunoglobulin heavy constant mu
Gene Synonym(s)	AI326478; BCR; Ig mu; IgM; Igh-6; Igh-M; Igh-M; Igh6; expressed sequence AI326478; immunoglobulin heavy chain 6 (heavy chain of IgM); immunoglobulin heavy chain mu; muH; muMT
Strain of Origin	129S2/SvPas
Chromosome	12
Molecular Note	A neomycin resistance cassette disrupted one of the membrane exons of the gene encoding immunoglobulin heavy chain of the class mu (IgM).
Mutations Made By	Daisuke Kitamura, University of Cologne

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Ighm^tm1Cgn related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - B cell deficiency
Research Tools
- Cancer Research
  - B cell deficiency
- Immunology, Inflammation and Autoimmunity Research
  - B cell deficiency

Mammalian Phenotype Terms by Genotype

Genotype: Ighm^tm1Cgn/Ighm⁺
NOD.129S2-Ighm^tm1Cgn

immune system phenotype

increased susceptibility to autoimmune diabetes
- 90% of female and 45% of male heterozygotes develop diabetes (glycosuric values >3) by 20 weeks of age compared to 0% of homozygotes

Genotype: Ighm^tm1Cgn/Ighm^tm1Cgn
NOD.129S2-Ighm^tm1Cgn/DvsJ

immune system phenotype

abnormal T cell number
- the proportion, but not the number, of CD 4 and CD8 T cells found in the spleen is increased due to the absence of B cells

abnormal T cell proliferation
- T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD

abnormal spleen B cell follicle morphology
- follicles do not develop in the spleen

absent B cells
- B cells are absent in the spleen

decreased susceptibility to autoimmune diabetes
- 13.6% of female mice develop diabetes by 21 weeks of age compared to control NOD mice that have an incidence rate of 95.5% at this age

hematopoietic system phenotype

abnormal T cell number
- the proportion, but not the number, of CD 4 and CD8 T cells found in the spleen is increased due to the absence of B cells

abnormal T cell proliferation
- T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD

abnormal spleen B cell follicle morphology
- follicles do not develop in the spleen

absent B cells
- B cells are absent in the spleen

Genotype: Ighm^tm1Cgn/Ighm^tm1Cgn
NOD.129S2-Ighm^tm1Cgn

immune system phenotype

decreased susceptibility to autoimmune diabetes
- no male or female homozygotes develop diabetes (assessed by glycosuric levels >3) by 20 weeks of age

References

Serreze DV; Chapman HD; Varnum DS; Hanson MS; Reifsnyder PC; Richard SD; Fleming SA; Leiter EH; Shultz LD. 1996. B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: analysis of a new speed congenic stock of NOD.Ig mu null mice. J Exp Med 184(5):2049-53. PubMed: 8920894 MGI: J:37287

Additional - Ighm^tm1Cgn related

Abraham D; Leon O; Schnyder-Candrian S; Wang CC; Galioto AM; Kerepesi LA; Lee JJ; Lustigman S. 2004. Immunoglobulin E and eosinophil-dependent protective immunity to larval Onchocerca volvulus in mice immunized with irradiated larvae. Infect Immun 72(2):810-7. PubMed: 14742524 MGI: J:87861
Akashi T; Nagafuchi S; Anzai K; Kitamura D; Wang J; Taniuchi I; Niho Y; Watanabe T. 1998. Proliferation of CD3+ B220- single-positive normal T cells was suppressed in B-cell-deficient lpr mice. Immunology 93(2):238-48. PubMed: 9616374 MGI: J:45808
Ali M; Weinreich M; Balcaitis S; Cooper CJ; Fink PJ. 2003. Differential regulation of peripheral CD4+ T cell tolerance induced by deletion and TCR revision. J Immunol 171(11):6290-6. PubMed: 14634147 MGI: J:132828
Allen HL; Deepe GS Jr. 2006. B cells and CD4-CD8- T cells are key regulators of the severity of reactivation histoplasmosis. J Immunol 177(3):1763-71. PubMed: 16849486 MGI: J:138028
Alpan O; Rudomen G; Matzinger P. 2001. The role of dendritic cells, B cells, and M cells in gut-oriented immune responses. J Immunol 166(8):4843-52. PubMed: 11290760 MGI: J:68620
Amante FH; Haque A; Stanley AC; Rivera Fde L; Randall LM; Wilson YA; Yeo G; Pieper C; Crabb BS; de Koning-Ward TF; Lundie RJ; Good MF; Pinzon-Charry A; Pearson MS; Duke MG; McManus DP; Loukas A; Hill GR; Engwerda CR. 2010. Immune-Mediated Mechanisms of Parasite Tissue Sequestration during Experimental Cerebral Malaria. J Immunol 185(6):3632-42. PubMed: 20720206 MGI: J:163540
Andersen C; Jensen T; Nansen A; Marker O; Thomsen AR. 1999. CD4(+) T cell-mediated protection against a lethal outcome of systemic infection with vesicular stomatitis virus requires CD40 ligand expression, but not IFN-gamma or IL-4. Int Immunol 11(12):2035-42. PubMed: 10590269 MGI: J:110491
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Andoh M; Zhang G; Russell-Lodrigue KE; Shive HR; Weeks BR; Samuel JE. 2007. T Cells Are Essential for Bacterial Clearance, and Gamma Interferon, Tumor Necrosis Factor Alpha, and B Cells Are Crucial for Disease Development in Coxiella burnetii Infection in Mice. Infect Immun 75(7):3245-55. PubMed: 17438029 MGI: J:122426
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Aroeira LS; Mouton CG; Toran JL; Ward ES; Martinez C. 1999. Anti-Vbeta8 antibodies induce and maintain staphylococcal enterotoxin B-triggered Vbeta8+ T cell anergy. Eur J Immunol 29(2):437-45. PubMed: 10064059 MGI: J:115226
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Arras M; Louahed J; Simoen V; Barbarin V; Misson P; van den Brule S; Delos M; Knoops L; Renauld JC; Lison D; Huaux F. 2006. B lymphocytes are critical for lung fibrosis control and prostaglandin E2 regulation in IL-9 transgenic mice. Am J Respir Cell Mol Biol 34(5):573-80. PubMed: 16424385 MGI: J:136512
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Ashour HM; Niederkorn JY. 2006. Peripheral tolerance via the anterior chamber of the eye: role of B cells in MHC class I and II antigen presentation. J Immunol 176(10):5950-7. PubMed: 16670303 MGI: J:131707
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