Search Criteria: Research Area is "Research Tools: Cancer Research: B cell deficiency"

New Strains Awaiting Transfer from the Donor
Additional Register Interest Strains

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
002288 B6.129S2-Ighmtm1Cgn/J
Level 2
Mice homozygous for the Ighmtm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B cells. There is no expression of membrane-bound IgM, although some B cells may be produced using a C gene other than mu. It may be useful as a model for B cell immunodeficiency found in humans. Also known as muMT.
002249 B10.129S2(B6)-Ighmtm1Cgn/J
Repository- Live
Mice homozygous for the Ighmtm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also know as muMT.
014175 B6(Cg)-Irf8tm1.1Hm/J
Repository- Live
These mice possess loxP sites on either side of exon 2, which encodes the DNA binding domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s).

When bred to a strain with Cre recombinase expression in B lymphocytes (see Stock No. 006785 for example), this mutant mouse strain may be useful in studies of B cell differentiation.

018298 B6(Cg)-Irf8tm1.2Hm/J
Repository- Live
Mice homozygous for this Irf8 knockout allele (Irf8-/-) may be expected to to exhibit some or all of the phenotype published for other Irf8 null mutations on both a C57BL/6J-congenic and mixed genetic background. For example, other Ifr8 null mice are viable and fertile as young animals. Homozygotes are immunodeficient (abnormal populations of B cells, T cells, granulocytes and macrophages) and develop a syndrome similar to human chronic myeloid leukemia. Acute onset begins by 10 weeks of age, progresses through chronic stage (~20 weeks of age), and significant mortality by ~50 weeks of age.

In an attempt to offer knockout versions of conditional alleles, The Jackson Laboratory Repository bred floxed mice (Stock No. 014175) with germline-expressing Cre recombinase mice (Stock No. 008454). The resulting animals with pan deletion of the floxe .....
For more information please see the full phenotype on the strain data sheet

008449 B6(Cg)-Rag2tm1.1Cgn/J
Repository- Live
These RAG-2del mutant mice harbor a pan deletion of exon 3 of the targeted locus. Homozygotes (RAG-2del/del) are viable and fertile, with pan deletion of the entire RAG-2 protein coding region. Homozygous mice may be expected to have the same knockout phenotype as other RAG-2 null mutants or similarly created RAG-2 exon 3 pan-deleted mutants; with hematopoietic and immune system defects including arrested B cell and T cell development at the pro-B and the pro-T cell stages, respectively. These RAG-2del mice may be useful in studying the role of RAG-2 in B cell and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was .....
For more information please see the full phenotype on the strain data sheet

011112 B6.129-Flt3tm1Dgg/J
Repository- Live
These mice carry the human W51 mutation, ITD, internal tandem duplication of amino acids 596 to 602, in the endogenous mouse Flt3 locus, which confers constitutive FLT3 signaling. Mice that are homozygous for the targeted mutation are viable and fertile. The Donating Investigator reports that BALB/c mice carrying this allele are not as viable as mutants on the C57BL/6 background. Although FLT protein levels are comparable to wildtype, increased phospho-Flt3 (p-FLT3) and phospho-Stat5 (pSTAT5) levels are detected by flow cytometric analysis of homozygous bone marrow and splenic cells. Homozygotes exhibit leukocytosis, monocytosis and progressive splenomegaly. Mature myeloid and monocytic populations in homozygotes are increased, with reduced B and T cell populations. B cell development is arrested at the pre-B stage. Heterozygotes have decreased liver size, hemoglobin levels, platelet counts and exhibit a milder maturing myeloid hyperplasia phenotype when compared to hom .....
For more information please see the full phenotype on the strain data sheet
007745 B6.Cg-Mir155tm1.1Rsky/J
Repository- Live
Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-α (LT-α) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreased percentage of interferon-γ (IFN-& .....
For more information please see the full phenotype on the strain data sheet
013115 B6.Cg-Rag1tm1Mom Tg(UBC-GFP)30Scha/J
Repository- Live
Rag1-deficient ubiquitin-GFP mice on the C57BL/6 genetic background (B6.Rag1-/-;UBC-GFP) combine lymphocyte-deficiency with widespread green fluorescent protein expression. Mice homozygous for both the Rag1 null allele and the UBC-GFP transgene (Rag1-/-;UBC-GFP+/+) are viable and fertile. Double homozygous mice produce no mature T cells or B cells, and have widespread GFP expression that is uniform within cell lineage. GFP expression varies between different cell types; hematopoetic cells have high expression levels compared with other cells. Red blood cells from UBC-GFP homozygotes should fluoresce at approximately twice the level compared to UBC-GFP hemizygotes.

Similar to other immunodeficient strains, maintaining Rag1-deficient mice in high health status (specific pathogen-free) vivaria promotes overall colony health. If Rag1-deficient animals are maintained in low health barrier rooms, the use of medicated water (sulf .....
For more information please see the full phenotype on the strain data sheet

008448 C.B6(Cg)-Rag2tm1.1Cgn/J
Repository- Live
These RAG-2del mutant mice harbor a pan deletion of exon 3 of the targeted locus. Homozygotes (RAG-2del/del) are viable and fertile, with pan deletion of the entire RAG-2 protein coding region. Homozygous mice may be expected to have the same knockout phenotype as other RAG-2 null mutants or similarly created RAG-2 exon 3 pan-deleted mutants; with hematopoietic and immune system defects including arrested B cell and T cell development at the pro-B and the pro-T cell stages, respectively. These RAG-2del mice may be useful in studying the role of RAG-2 in B cell and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was .....
For more information please see the full phenotype on the strain data sheet

008309 C57BL/6-Rag2tm1Cgn/J
Repository- Live
Mice homozygous for the RAG-2fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research.

For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development.

006608 NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ
Repository- Live
NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ (NOD.IgHEL Ighm-deficient) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Because these mice are Ighm-deficient, they do not express endogenous IgM. All B lymphocytes in NOD.IgHEL Ighm-deficient mice express Ig molecules specific for hen egg lyzozyme (HEL). There is no significant difference in the total number of B and T lymphocytes between NOD.IgHEL Ighm-deficient and NOD.IgHEL (Stock No. 006345) mice. The incidence of diabetes in transgenic vs. non-transgenic NOD.Ighm-deficient mice is similar by 21 weeks of age, (16.7% vs. 13.6%, respectively). Histological evaluation of 12 week old NOD.IgHEL Ighm-deficient mice shows that most mice have low levels of insulitis compared to NOD/ShiLt control mice, although an occasional animal had extensive insulitis. In additio .....
For more information please see the full phenotype on the strain data sheet
021885 NOD.Cg-Prkdcscid H2-Ab1tm1Gru Il2rgtm1Wjl/SzJ
Repository- Live
NSG-Abo mice are NOD.scid.Il2Rγcnull ("NSG"; Stock No. 005557) animals also harboring the H2-Ab1tm1Gru knockout allele (Abo). NSG-Abo females homozygous for all three mutations, and males homozygous for scid, homozygous for Abo and hemizygous for the X-linked Il2Rγcnull may be collectively referred to as homozygous NSG-Abo mice.

Although viable and fertile, homozygous NSG-Abo mice are immunodeficient: they have no mature T cells or B cells, lack functional natural killer (NK) cells, are deficient in cytokine signaling, and do not express murine major histocompatibility complex (MHC) class II (lack cell surface expression of both class II-A and class II-E MHC proteins). While both homozygous NSG and homozygous NSG-Abo mice readily allow engraftment of purified human CD4> .....
For more information please see the full phenotype on the strain data sheet

017914 NOD.Cg-Rag1tm1Mom Il2rgtm1Wjl Tg(HLA-DRA,HLA-DRB1*0401)39-2Kito/ScasJ
Repository- Live
DRAG mice are NOD.Rag1KO.IL2RγcKO ("NRG"; Stock No. 007799) animals with chimeric human-mouse class II transgenes encoding the HLA class II antigen binding domain molecules (defined by the HLA-DR4 genotype [HLA-DRA/HLA-DRB1*0401]) fused to the I-Ed MHC class II molecule. The presence of these HLA-DR4-IE transgenes allows irradiated DRAG mice to be engrafted with HLA-DR-matched hematopoietic stem cells (HSC); resulting in humanized T cell and B cell populations.

DRAG females homozygous for both mutations and homozygous for the co-injected transgenes (and DRAG males homozygous for the Rag1KO mutation; hemizygous for the X-linked IL2RγcKO mutation; homozygous for the co-injected transgenes) are viable and fertile, with no mature T cells, B cells, or natural killer (NK) cells. Like NRG mice, DRAG mice have the same irradiation/engraftment advantages compared to NOD.scidKO.IL2RγcKO ("NSG"; Sto .....
For more information please see the full phenotype on the strain data sheet

014543 STOCK Hgftm1.1(HGF)Aveo Prkdcscid/J
Repository- Live
Mice homozygous for both the hHGFki and Prkdcscid alleles, also called immunocompromised hHGFki mice, are viable and fertile.

The hHGFki allele is a "humanized" knock-in mutation that replaces the mouse hepatocyte growth factor (HGF) coding region downstream of the signal sequence with the human HGF cDNA sequence. As a result, the endogenous mouse promoter drives expression of human HGF. While the human HGF activates both the human and murine form of its tyrosine kinase receptor (met proto-oncogene (MET; c-Met)), the murine HGF is unable to activate human MET. Mice homozygous for hHGFki express only the human form of HGF. In homozygous hHGFki mice, HGF expression from the knock-in allele is observed in developing embryo, as well as adult liver, kidney and lung. hHGFki homozygous mice exhibit an increase in serum HGF after clotting.

Mice homozygous for the Prkdcscid mutation exhibit T- and B-cell deficiency.

021571 BXSB.129S7(B6)-Rag1tm1Mom/DcrJ
Under Development - Now Accepting Orders
Rag1-deficient BXSB.Yaa mice (BXSB.Rag1-/- or BXSB.Yaa Rag1-/-) are a BXSB/MpJ-congenic strain carrying a null mutation of the recombination activating gene 1.

BXSB/MpJ inbred males (Stock No. 000740) develop a spontaneous lupus-like autoimmune syndrome: mortality starts at ~13 weeks of age with 50% lethality by ~30 weeks and 76% lethality by ~40 weeks. BXSB/MpJ inbred females develop a greatly attenuated form of autoimmune disease because they lack Yaa.

Homozygous (Rag1-/-) mice are viable and fertile. Homozygotes produce no mature T cells or B cells, and should be maintained in pathogen-free conditions on sulfatrim water to increase colony health (similar to other immunodeficient strains). Compared to BXSB/MpJ, the lymphocyte-deficiency of BXSB.Rag1-/- mice prevents manifestation of the spontaneous autoimmune phenotype in both males and females.

Heterozygous males (BXSB.Rag1+/-) develop the BXSB .....
For more information please see the full phenotype on the strain data sheet

023848 NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-D1tm1Bpe Il2rgtm1Wjl/SzJ
Under Development - Now Accepting Orders
NSG-(KbDb)null mice are NOD.scid.Il2Rγcnull ("NSG"; Stock No. 005557) animals also harboring knockout alleles of the MHC class I genes (Kb null and Db null). NSG-(KbDb)null females homozygous for all three mutations, and males homozygous for scid, homozygous for Kb null, homozygous for Db and hemizygous for the X-linked Il2Rγcnull may be collectively referred to as homozygous NSG-(KbDb)null mice.

Although viable and fertile, homozygous NSG-(KbDb)null mice are immunodeficient: they have no mature T cells or B cells, lack functional natural killer (NK) cells, are deficient in cytokine signaling, and do not express murine major histocompatibility complex (MHC) class I molecules (lack classi .....
For more information please see the full phenotype on the strain data sheet

024099 NOD.Cg-Rag1tm1Mom Il2rgtm1Wjl Tg(CMV-IL3,CSF2,KITLG)1Eav/J
Under Development - Now Accepting Orders
NRGS (NRG-SGM3) mice are NOD.Rag1-;γcnull (NRG) animals also carrying the SGM3 (3GS) triple coinjected transgenes that express human interleukin-3 (IL-3), human granulocyte/macrophage-stimulating factor (GM-CSF) and human Steel factor (SF).

NRGS females homozygous for both mutations and homozygous for the 3GS triple coinjected transgenes (and NRGS males homozygous for the Rag1- mutation, hemizygous for the X-linked ;γcnull mutation and homozygous for the 3GS triple coinjected transgenes) are viable and fertile, with no mature T cells, B cells, or natural killer (NK) cells. Like NOD.Rag1-/-;γcnull mice (NRG; Stock No. 007799), these NRGS mice have the same irradiation/engraftment advantages over NOD.scid ;γcnull (NSG; Stock No. 005557) .....
For more information please see the full phenotype on the strain data sheet

004524 B6.129-Blnktm1Achn/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of bone marrow-derived cell lysates. There is a 65% reduction of splenocyte number. Development of B lymphocytes is arrested at the B220+CD43+ progenitor B cell to B220+CD43- precursor B cell transition stage. The reduced number of mature peripheral B-cells results in diminished serum Ig levels in adult homozygous mice. Peritoneal CD5+IgM+ B-1a B-cell numbers are decreased. This mutant mouse strain may be useful in studies of agammaglobulinemia.
010572 B6.129S2-Tnfsf13btm1Msc/J
Cryopreserved - Ready for recovery
Homozygous (BAFF-/- or BAFF KO) mice are viable and fertile. The BAFF knockout mutation has a tailless human CD2 reporter gene inserted into the Tnfsf13b (BAFF) locus that abolishes endogenous BAFF expression. Homozygous mice exhibit abnormal B cell development and function, resulting from significant loss of mature B cell (B220+) populations in lymph nodes, peripheral blood and bone marrow, as well as attenuated antibody responses to both T cell-dependent and T cell-independent type II antigens. Homozygous also have splenic deficiencies (mass, marginal zone B cells and follicular B cells), and decreased total serum immunoglobulin in each subclass (with the exception of immunoglobulin A [IgA] which was only moderately reduced). No loss of marrow pre-B cells, marrow pro-B cells, or CD3+ T cells are reported with BAFF-deficiency. Heterozygous mice have moderately reduced serum IgG subclasses and IgM. These BAFF-mutant mice may be useful in studyin .....
For more information please see the full phenotype on the strain data sheet
004197 B6.129S6-Rac2tm1Mddw/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu .....
For more information please see the full phenotype on the strain data sheet
010914 B6.Cg-Tg(Emu-TXLNA)1Amjr/J
Cryopreserved - Ready for recovery
Mice harboring the pEμSR-IL-14α transgene are viable and fertile, with expression of hemagglutinin-tagged human IL-14α (TXLNA or taxilin alpha) directed predominantly to the B lymphocyte compartment by the Eμ immunoglobulin heavy chain enhancer/SV40 promoter regions (from the pEμSR vector). Human IL-14α expression levels from the transgene are similar to mouse IL-14α expression levels observed in activated T cells/B cells. Transgene expression results in a phenotype with characteristics of systemic lupus erythematosus (SLE) and Sjogren's syndrome. Specifically, transgenic mice exhibit hypergammaglobulinemia (enhanced responses to T-dependent and T-independent antigens), autoantibodies, sialadenitis (infiltration of the parotid glands with lymphocytes), and mild immune-complex mediated nephritis with glomerular IgM deposition. In addition, almost all aged IL-14α-transgenic mice develop large B cell lymphoma (CD5+ B cell lymphoma) similar to .....
For more information please see the full phenotype on the strain data sheet
013598 B6;129-Tcf4tm1Zhu/J
Cryopreserved - Ready for recovery
A targeting vector was designed to replace the C-terminus DNA-binding domain of transcription factor 4 (Tcf4 or E2-2) gene with a neomycin (neo) selection cassette. Homozygotes are born at a low frequency and die within the first week of life. E2-2 is a widely expressed E2A-related helix-loop-helix (HLH) protein required for the generation of normal numbers of pro-B cells in mouse embryos. While homozygous E2-2 mutant embryos are capable of making B cells, they produce only half as many as wildtype. When crossed to mice containing a (Atoh1)-lacZ transgene, β-galactosidase staining is evident in anterior extramural migratory stream (AES) cells which accumulate in the region lateral to the pontine nucleus. The resulting mice exhibit a reduction in size of the pontine nucleus and a lack of migration of neuronal precursors to the region of the pontine nucleus. Mice heterozygous for the mutation are viable, fertile, and normal in size. This strain may be .....
For more information please see the full phenotype on the strain data sheet
002536 B6;129S-Btktm1Wk/J
Cryopreserved - Ready for recovery
Mice homozygous for the Btktm1Wk targeted mutation are viable and fertile. Homozygous mutant mice show defects in B-cell maturation and activation. This strain has the same phenotype as the spontaneous X-linked immune deficiency mutation (CBA/CaHN-Btkxid/J; Stock No. 001011). See Inbred Strain listing.
003751 B6;129S4-Ighmtm1Che/J
Cryopreserved - Ready for recovery
Mice homozygous for the Ighmtm1Che allele are viable, fertile and exhibit no apparent defects. While membrane expressed Ighmtm1Che is unhindered, these mice are unable to produce the secreted form of Ighmtm1Che. Increases in some classes of serum Ig is noted in young animals (IgA, IgG2a and IgG3), but these differences are largely absent in the adult animals. The IgG1 antibody response to suboptimal doses of a T cell-dependent antigen is impaired. Conversely, the IgG2a antibody response to a T cell-independent antigen appears augmented. An approximately three-fold increase in B-1 lymphocytes is noted in the spleen and peritoneum.
021871 BXSB.129S2(B6)-Ighmtm1Cgn/DcrJ
Cryopreserved - Ready for recovery
Ighm-deficient BXSB.Yaa mice (BXSB.Ighm-/- or BXSB.Yaa Ighm-/-) are a BXSB/MpJ-congenic strain carrying a null mutation of the immunoglobulin heavy chain of the class mu.

BXSB/MpJ inbred males (Stock No. 000740) develop a spontaneous lupus-like autoimmune syndrome: mortality starts at ~13 weeks of age with 50% lethality by ~30 weeks and 76% lethality by ~40 weeks. BXSB/MpJ inbred females develop a greatly attenuated form of autoimmune disease because they lack Yaa.

Homozygous (Ighm-/-) mice are viable and fertile. Homozygotes lack mature B cells and have no expression of membrane-bound IgM; although some B cells may be produced using immunoglobulin genes other than mu. As such, they should be maintained in pathogen-free conditions on sulfatrim water to increase colony health (similar to other immunodeficient strains). Compared to BXSB/MpJ, the mature B cell-deficiency of BXSB.Ighm-/- mice prevents manif .....
For more information please see the full phenotype on the strain data sheet

004349 C.129S2-Ighmtm1Cgn/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Homozygous mice lack B220+ peripheral blood lymphocytes. This mutant mouse strain represents a model that may be useful in studies related to B-cell immunodeficiency.
007707 C57BL/6-Itgb7tm1Mshi/J
Cryopreserved - Ready for recovery
Mice homozygous for this β7 (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted β7 integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the β7 integrin head (A-domain). The resulting imbalance between the non-adhesive and adhesive states of leukocyte integrins skews toward a persistently adhesive state. Homozygous mutants exhibit impaired leukocyte migration, perturbed lymphocyte trafficking in the gut, and reduced T- and B-cell numbers in small/large bowel and gut-associated lymphoid tissues (less T-cells in Peyer's patches (PP), fewer intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) compartments in the small intestine; and less B-cells in PP and the large intestine). In addition, CD4+CD45RBhigh T cells isolated fro .....
For more information please see the full phenotype on the strain data sheet
008338 CByJ.B6(Cg)-Rag2tm1Cgn/J
Cryopreserved - Ready for recovery
Mice homozygous for the RAG-2fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research.

For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development.

In an attempt to offer alleles on well-characterized or multiple genetic background .....
For more information please see the full phenotype on the strain data sheet

004639 NOD.129S2(B6)-Ighmtm1Cgn/DoiJ
Cryopreserved - Ready for recovery
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 dependant 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)
004848 NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/SzJ
Cryopreserved - Ready for recovery
Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1tm1Mom/J (Stock No. 003729). Although an increased number of DX5+CD122+ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho .....
For more information please see the full phenotype on the strain data sheet
005309 NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ
Cryopreserved - Ready for recovery
Transgenic mice carrying the Ighmtm1Cgn allele are viable, fertile, and normal in size and restores the B220+ B-cells. The number of B-cells is reduced and the ratio of CD4 to CD8 is normal. Although only a fraction of the transgenic mice have an increased amount of insulitis, it is significantly more severe, especially in males. No diabetes was observed in NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ mice by 50 weeks of age.

This model serves as a control for the membrane bound, non-secreted, NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ (Stock No. 005306).

005306 NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ
Cryopreserved - Ready for recovery
Transgenic mice carrying the Ighmtm1Cgn allele are viable, fertile, and normal in size and restores the B220+ B-cells to normal. The number of B-cells is normal and the ratio of CD4 to CD8 is normal. Although only a fraction of the transgenic mice have an increased amount of insulitis, it is more severe, especially in males. Diabetes incidence is partially restored in NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/Fsw with approximately, 11% females and 0% males becoming diabetic by 50 weeks of age compared to approximately 2% Ighmtm1Cgn female controls and 0% Ighmtm1Cgn male controls by 50 weeks of age or 90% female NOD controls and 70% male NOD controls by 30 weeks of age. T- cell depleted spleen cells from Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk mice stimulated with lipopolysaccharide (LPS) respond normally. NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m )2Mjsk/Fsw like NOD.129S2(B6)-<> .....
For more information please see the full phenotype on the strain data sheet
003903 NOD.129S2-Ighmtm1Cgn/Dvs
Research Strain
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)

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New Strains Awaiting Transfer from the Donor

(See informational text following listing of strains)
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

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Stock
Number
Strain Name
 
Strain Description
Standard Supply
024511B6.Cg-Tcf12tm3Zhu Tcf3tm4Zhu/J
Awaiting Transfer from the Donor
HEBf E2Af mice allow Cre-recombinase inducible deletion of the two basic helix-loop-helix (bHLH) E-protein family genes HEB and E2A. These mice may be useful for studying B and T lymphocyte development and lymphoid malignancies.
017712C;129S4-Rag2tm1.1Flv Csf1tm1.1(CSF1)Flv Csf2/Il3tm1.1(CSF2,IL3)Flv Thpotm1.1(TPO)Flv Il2rgtm1.1Flv Tg(SIRPA)1Flv/J
Awaiting Transfer from the Donor
MISTRG are Rag2-deficient, Il2rg-deficient mice with human versions of four cytokines important for innate immune cell development (M-CSFh;IL-3/GM-CSFh;hSIRPAtg;TPOh;Rag2-;γc-). MISTRG mice are highly permissive for human hematopoiesis; supporting the development and function of monocytes, macrophages and NK cells derived from human fetal liver or adult CD34+ progenitor cells. MISTRG is a humanized mouse for modelling the human immune system in scenarios of health and pathology, such as human cell engraftment and patient-derived tumor xenografts (PDX).
017711C;129S4-Rag2tm1.1Flv Csf1tm1.1(CSF1)Vlcg Csf2/Il3tm1.1(CSF2,IL3)Flv Thpotm1.1(TPO)Flv Il2rgtm1.1Flv/J
Awaiting Transfer from the Donor
MITRG are Rag2-deficient, Il2rg-deficient mice with human versions of three cytokines important for innate immune cell development (M-CSFh;IL-3/GM-CSFh;TPOh;Rag2-;γc-). MITRG mice are highly permissive for human hematopoiesis; supporting the development and function of monocytes, macrophages and NK cells derived from human fetal liver or adult CD34+ progenitor cells. MITRG is a humanized mouse for modelling the human immune system in scenarios of health and pathology, such as human cell engraftment and patient-derived tumor xenografts (PDX).

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New Strains Awaiting Transfer from the Donor
  • Receive periodic updates on the status of the colony AWAITING TRANSFER
  • Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
  • Provide input affecting speed and quantity of availability
The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.

It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

Additional Register Interest Strains

Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

View a Data sheet for a Strain
Select the strain name to link to the strain data sheet.

Stock
Number
Strain Name
 
Strain Description
Standard Supply
014553NOD.Cg-Hgftm1.1(HGF)Aveo Prkdcscid Il2rgtm1Wjl/J
In Progress
NSG-hHGFki mice are NOD.scid.Il2Rγcnull ("NSG") animals with the Hgftm1.1(HGF)Aveo "humanized" knock-in allele (hHGFki). Homozygous NSG-hHGFki mice have no mature T cells or B cells, lack functional natural killer (NK) cells, are deficient in cytokine signaling, and express human hepatocyte growth factor (HGF) in place of the endogenous mouse HGF. These mice may be useful in studying the HGF/MET pathway in human tumor xenografts and mouse tumor allografts, as well as examining the ability of anti-HGF to inhibit angiogenesis and other tumor/stroma interactions.

(1 stocks)         Back to Top


It is VERY IMPORTANT that you Register Interest. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain.

Send questions to our Technical Support team using the Express Technical Support Form.
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