JAX Mice Database - T Cell Receptor Signaling Defects

Search Criteria: Research Area is "Immunology and Inflammation Research: T Cell Receptor Signaling Defects"

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JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002216	B6.129S7-Rag1^tm1Mom/J	Level 3
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor-positive. Neither the spleen nor the bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
003303	C.Cg-Tg(DO11.10)10Dlo/J	Level 3
	Mice carrying the MHC class II restricted rearranged T cell receptor transgene, Tg(DO11.10)10Dlo, react to ovalbumin (OVA) peptide antigen. Intraperitoneal administration of OVA to transgenic mice results in a rapid deletion of the immature CD4⁺ CD8⁺ TCR^lo thymocytes with progression to mature thymocytes. Apoptosis of cortical thymocytes within 20 hours of treatment indicates that apoptosis in important in the development of antigen-induced tolerance. Use of this rearranged T cell receptor transgene requires H2^d background.
004194	C57BL/6-Tg(TcraTcrb)425Cbn/J	Level 3
	These transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand. These transgenic mice are useful for studying in vivo T-cell biology such as TCR-ligand interactions, T-cell activation, thymic selection, cross-presentation of antigens, process of thymic selection and central and peripheral T-cell tolerance and induction.
002118	B6.129P2-Tcrb^tm1Mom/J	Level 4
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8^- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002120	B6.129P2-Tcrd^tm1Mom/J	Level 4
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
002116	B6.129S2-Tcra^tm1Mom/J	Level 4
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full descriiption on the strain data sheet
003145	C.129S7(B6)-Rag1^tm1Mom/J	Level 4
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL-2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or wildtype siblings.
003831	C57BL/6-Tg(TcraTcrb)1100Mjb/J	Level 4
	These mice contain transgenic inserts for mouse Tcra-V2 and Tcrb-V5 genes. The transgenic T cell receptor was designed to recognize ovalbumin residues 257-264 in the context of H2K^b and used to study the role of peptides in positive selection and the response of CD8⁺ T cells to antigen. Like most TCR transgenics, these mice are somewhat immunodeficient.
002761	B10.Cg-Tg(TcrAND)53Hed/J	Repository- Live
	Mice carrying the (TcrAND)53Hed transgene express a rearranged T-cell receptor (V alpha 11.1 / V beta 3) specific for the carboxy-terminal fragment of pigeon cytochrome c and the E^k molecule, resulting in a major subpopulation of T cells restricted to class II MHC proteins. There are an abnormally high percentage of mature CD4⁺CD8^- cells. The peripheral T-cell population is almost exclusively CD4⁺. The original C57BL/6 and SJL mixed background strain (Stock number 002408) was backcrossed to C57BL/10 to create this strain. Both strains are fixed for H2^b. Because C57BL/10 mice do not express I-E, this mouse must be crossed to a strain that expresses I-E^k to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. The lack of I-E^k expression in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing I-E^k< > ..... For more information please see the full descriiption on the strain data sheet
002122	B6.129P2-Tcrb^tm1Mom Tcrd^tm1Mom/J	Repository- Live
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full descriiption on the strain data sheet
002762	B6.129S2-Irf1^tm1Mak/J	Repository- Live
	Mice homozygous for the Irf1^tm1Mak targeted mutation are viable and fertile with no major abnormalities. T cell development is impaired leading to significant reduction in TCR alpha beta ⁺ CD4^- CD8⁺ T cells. Type I interferon gene induction is abnormal.
008076	B6.129S4-Traf1^tm1Tsi/J	Repository- Live
	Mice homozygous for the TRAF1 mutant allele (TRAF1^-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1^-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1^-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bim_s. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1^-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1^-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el ..... For more information please see the full descriiption on the strain data sheet
004088	B6.Cg-Foxp3^sf/J	Repository- Live
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3^sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3^sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3^sf/Y mice do not develop scurfy ..... For more information please see the full descriiption on the strain data sheet
004369	B6.Cg-Rag1^tm1Mom Ins2^Akita/J	Repository- Live
	Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age.
005023	B6.Cg-Thy1^a/Cy Tg(TcraTcrb)8Rest/J	Repository- Live
	This transgenic strain carries a rearranged T cell receptor transgene specific for the mouse homologue (pmel-17) of human SILV (gp100), an enzyme involved in pigment synthesis that is expressed by the majority of malignant melanoma cells including B16 melanoma, as well as by normal melanocytes. The strain is also homozygous for the T lymphocyte specific Thy1^a (Thy1.1) allele. CD8+ T cells express a Tcra-V1/Tcrb-V13- transgenic TCR that recognizes an epitope of pmel-17 corresponding to amino acids 25-33 of gp100 presented by H2-D^b MHC class I molecules. Greater than 95% of the CD8+ T cells in transgenic mice expressed the transgenic TCR based on the expression of Vbeta13, amounting to about 20% of all splenocytes. T cells in blood and spleen generally expressed baseline levels of the activation/effector markers CD25, CD44, and CD69, indicating that most of the transgenic cells were in the naive state. These transgenic mice in conjunction with the poor ..... For more information please see the full descriiption on the strain data sheet
002385	B6;129S7-Fyn^tm1Sor/J	Repository- Live
	Mice homozygous for the Fyn^tm1Sor targeted mutation are viable and fertile displaying no overt phenotype. T cell receptor signaling is defective in homozygous mutant mice and are characterized by a reduction in levels of tyrosine-phosphorylated proteins, failure to flux calcium in response to TCR cross-linking, and a reduction in production of calcium-related IL2. THY-1-induced proliferation is also reduced in thymocytes but not in splenic T cells. Neurological defects include blunted long-term potentiation (LTP), impaired special learning, and altered hippocampal development.
002096	B6;129S7-Rag1^tm1Mom/J	Repository- Live
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
006912	C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J	Repository- Live
	Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4⁺ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco ..... For more information please see the full descriiption on the strain data sheet
008312	CBy.129P2(B6)-Tcrd^tm1Mom/SzJ	Repository- Live
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. 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 first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
005307	CBy.Cg-Thy1^a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Repository- Live
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I moleculeH2-K^d. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8⁺ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8⁺ T cells react with the HA peptide presented by H2-K^d. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This mouse is further modified with the Thy1.1 allele, rather than the alternate allele present in C57BL/10, DBA/2, and BALB/c mice. T ..... For more information please see the full descriiption on the strain data sheet
003729	NOD.129S7(B6)-Rag1^tm1Mom/J	Repository- Live
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency. (Prkdc^scid/Prkdc^scid) mice produce some B cells and IgM. NOD.129S7(B6)-Rag1^tm1Mom/J mice have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice is severely involuted. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that both B cell and T cell development have been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. Notable differences between this strain and the NOD.CB17-Prkdc^scid/J strain (Stock No. 001303) include a longer life s ..... For more information please see the full descriiption on the strain data sheet
007840	NOD.Cg-Prkdc^scid Tg(Ins2-CD86)12B70Flv/FswJ	Repository- Live
	Tg(Ins2-CD86)12B7 mice homozygous for the Prkdc^scid mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice express the human CD86 T cell co-stimulatory protein under the control of the rat insulin promoter (Ins2). RT-PCR analysis detects human CD86 mRNA expression in the pancreas. Very low expression levels are also detected in the kidney and thymus of some but not all transgenic mice. Immunohistochemistry indicates that transgenic CD86 protein expression is restricted to the Islets of Langerhans. Transgenic, Prkdc^scid homozygous mice lack functional T cells and B cells, and do not become diabetic. In the absence of the Prkdc^scid mutation, NOD-Tg(Ins2-CD86), transgenic mice experience accelerated diabetes. Diabetes onset in male and female transgenic NOD-Tg(Ins2-CD86) mice starts at 8 weeks of age and 85-90% of the mice ultimately become d ..... For more information please see the full descriiption on the strain data sheet
004848	NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/SzJ	Repository- Live
	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)-Rag1^tm1Mom/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 descriiption on the strain data sheet
007799	NOD.Cg-Rag1^tm1Mom Il2rg^tm1Wjl/SzJ	Repository- Live
	Females homozygous for both the Rag1^null and IL2rγ^null mutations (and males homozygous for Rag1^null and hemizygous for the X-linked IL2rγ^null mutation) are viable and fertile. When compared to NOD-scid IL2rg^null (Stock No. 005557), these NOD-Rag1^null IL2rγ^null mice tolerate much higher levels of irradiation conditioning. Additionally, NOD-Rag1^null IL2rγ^null mice support higher levels of both human cord blood stem cell engraftment following irradiation-conditioning (leading to multi-lineage hematopoietic cell populations and a complete repertoire of human immune cells, including human T cells) and human peripheral blood mononuclear cells engraftment in unconditioned adult mice with respect to NOD-Rag1^null (Stock No. For more information please see the full descriiption on the strain data sheet
004460	NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ	Repository- Live
	NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ mice carry both rearranged TCR alpha and beta genes from the cytotoxic CD4+ T cell clone BDC-2.5. When paired with a homozygous Rag1^tm1Mom mutation (such as in Stock No. 003729), recombination of endogenous TCR and Ig is prevented so that mature T cells in these mice express only the BDC2.5 TCR. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/ShiLtJ controls (12% incidence at age 30 weeks). When coupled with the homozygous Rag1^tm1Mom mutation, mice develop diabetes extremely early (mean age of 25 days). (Katz et al 1993, Gonzalez et al 2001, Mombaerts et al 1992)
005868	NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ	Repository- Live
	NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ, commonly called 8.3-NOD, express rearranged Tcra and Tcrb transgenes derived from the pancreatic beta cell-cytotoxic CD8⁺ T cell clone NY8.3. CD4^-CD8⁺ thymocytes and lymph derived T cells are skewed toward VB8.1/2⁺ expression when compared to wild type controls. Although, transgenic mice exhibit dramatically accelerated diabetes, the cumulative diabetes incidence and kinetics of disease are remarkably similar to their wild type cohorts. Insulitis scores of 3 week old transgene⁺ mice was significantly lower, while insulitis scores of 6 week olds were significantly more severe than in wild types controls, Verdaguer J et al, 1997, J. Exp Med 186, 1663-1676. Transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8⁺ T lymphocytes contributing to th ..... For more information please see the full descriiption on the strain data sheet
006770	STOCK Rag1^tm1Mom Tg(TIE2GFP)287Sato/J	Repository- Live
	To generate this double mutant strain, B6.Cg-Tg(TIE2GFP)287Sato/1J (Stock No. 004659) was crossed to C.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003145). This mutant mouse strain may be useful in studies examining angiogenesis in transplanted tissues. 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 first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described for each single mutant. We will modify the strain description if necessary as published results become available.
002271	129-Fyn^tm1Sor/J	Repository-Cryopreserved
	Mice homozygous for the Fyn^tm1Sor targeted mutation are viable and fertile displaying no overt phenotype. T cell receptor signaling is defective in homozygous mutant mice and are characterized by a reduction in levels of tyrosine-phosphorylated proteins, failure to flux calcium in response to TCR cross-linking, and a reduction in production of calcium-related IL2. THY-1-induced proliferation is also reduced in thymocytes but not in splenic T cells. Neurological defects include blunted long-term potentiation (LTP), impaired special learning, and altered hippocampal development.
003292	129S6/SvEvTac-Was^tm1Sbs/J	Repository-Cryopreserved
	WAS-deficient mice are viable and fertile. Mutant mice show normal lymphocyte development, serum immunoglobulin (Ig) levels and antibody responses. However, peripheral blood lymphocyte counts and platelet numbers are reduced in these mice. Development of chronic colitis is also observed. In vitro, WAS-deficient T cells show markedly impaired proliferative responses to anti-CD3e mediated stimulation. The Was gene is X-linked, so hemizygous males are WAS deficient.
005308	B10.Cg-H2^d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-K^d. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-K^d. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This transgenic model is useful in the study of T-cell activation, cross presentation of antigens, process of thymic selection, peripheral tolerance and ..... For more information please see the full descriiption on the strain data sheet
005534	B10.Cg-H2^d Tg(Ins2-HA)165Bri/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Mice homozygote for the transgene have silver grey fur color. Hemizygous and wildtype mice are black. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control m ..... For more information please see the full descriiption on the strain data sheet
005895	B10.Cg-Thy1^a H2^d Tg(TcraCl1,TcrbCl1)1Shrm/J	Repository-Cryopreserved
	Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA_518-526) restricted by MHC class I H-2K^d. Flow cytometric analysis shows appropriate skewing towards the CD8⁺ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8⁺ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th ..... For more information please see the full descriiption on the strain data sheet
003147	B10.D2-Hc¹ H2^d H2-T18^c/nSnJ-Tg(DO11.10)10Dlo/J	Repository-Cryopreserved
	Clonal deletion of autoreactive T cells in vivo was studied using a peptide antigen to induce deletion of antigen-reactive thymocytes. Mice transgenic for a T cell receptor that reacts to this peptide (Tg(DO11.10)10Loh) contain thymocytes that progress from the immature to the mature phenotype. Intraperitoneal administration of the peptide antigen to transgenic mice results in a rapid deletion of the immature CD4⁺ CD8⁺ TCR^lo thymocytes. Apoptosis of cortical thymocytes can be seen within 20 hours of treatment. These results provide direct evidence for the in vivo role of apoptosis in the development of antigen-induced tolerance.
003199	B10.PL-H2^u H2-T18^a/(73NS)Sn-Tg(TCRA)B1Jg/J	Repository-Cryopreserved
	TCR-transgenic mice exhibit the generation of an unusual population of CD4^-CD8^-TCR⁺ thymocytes and the absence of gamma delta cells. Transgenic TCR alpha chain causes thymocytes to differentiate into a CD4^-CD8^-TCR⁺ lineage at an early developmental stage, depleting the number of thymocytes that differentiate into the alpha-beta lineage. This transgene is also associated with the development of T cell lymphosarcoma. In combination with the transgenic strain TCR beta, it can be used as a model for Multiple Sclerosis.
003200	B10.PL-H2^u H2-T18^a/(73NS)Sn-Tg(TCRB)C14Jg/J	Repository-Cryopreserved
	TCR-transgenic mice exhibit the generation of an unusual population of CD4^-CD8^-TCR⁺ thymocytes and the absence of gama delta cells. Transgenic TCR beta chain causes immature T cells to accelerate differentiation into the alpha-beta lineage and thus inhibits the generation of gamma-delta cells. In combination with the transgenic strain TCR alpha, it can be used as a model for Multiple Sclerosis.
005711	B6.129P2-Prkcq^tm1Litt/J	Repository-Cryopreserved
	Mice homozygous for the targeted allele are viable, fertile, normal in size, and do not display any behavioral abnormalities. No endogenous or truncated protein product was detected in thymocytes or T cells. Mature T lymphocytes from null mice have blunted proliferative responses with decreased levels of both IL-2 and IL-2 receptor, and defective T cell receptor-initiated IkappaB-degradation/NF-kappaB activation. Homozygous mice exhibit severely impaired Th2, but normal Th1, immune responses as well as abnormal insulin signaling and glucose transport. Mutant mice also have defective regulatory T cell development (very low CD25 expression). This mutant may be suitable for use in studies related to T cell proliferation/signal transduction/immunodeficiency, Th2-mediated disease, asthma, and diabetes.
007015	B6.129S1-Gadd45g^tm1Flv/J	Repository-Cryopreserved
	Homozygotes are viable and fertile, but are poor breeders. TH1 helper T cells from homozygotes are severely compromised in their abilities to activate p38 (MAPK14)and JNK (MAPK8) in response to T cell receptor (TCR) signaling, produce much less interferon gamma (IFNG) upon restimulation, and are deficient in activation-induced cell death (AICD). Deficiencies in this gene also cause reduced contact hypersensitivity in the animals.
004197	B6.129S6-Rac2^tm1Mddw/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
005655	B6.Cg-Tg(Tcra,Tcrb)3Ayr/J	Repository-Cryopreserved
	This transgenic strain carries a rearranged T cell receptor that recognizes a complex consisting of a short peptide derived from the H2-Ea gene (Ealpha52-68) and the H2-Ab gene product (IA^b). This mouse lacks naturally occurring Ealpha52-68 peptide as the H2-Ea gene in C57BL/6J mice is incapable of expressing a protein product. Flow cytometric analysis shows 90% and 95% of CD4+ splenocytes expressing Tcra-V2 and Tcrb-V6, respectively. Mice that are hemizygous for these transgenes are viable, fertile and normal in size. This mutant mouse may be useful in studies of positive/negative selection, T cell receptor interactions, or graft-versus-host disease.
008428	B6.Cg-Tg(Tcra,Tcrb)HRCAll/J	Repository-Cryopreserved
	HRC transgenic mice express a transgene encoding a T cell receptor (TCR) αβ heterodimer specific for histone H4 (86-92) peptide VVYALKR presented by the H-2K^b class I MHC molecule. The TCRαβ transgene is expressed on >90% of mature T cells. Mice that are hemizygous for the transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. This mouse strain may be useful for studies of immune regulation, cancer, and autoimmunity.
008006	B6.Cg-Tg(Tcra51-11.5,Tcrb51-11.5)AR206Ayr/J	Repository-Cryopreserved
	Mice homozygous for this transgene are viable and fertile and do not display any gross physical or behavioral abnormalities. These transgenic mice carry a T cell receptor transgene specific for human class II-associated invariant chain peptide (CLIP)/I-A^b complexes. On a RAG-deficient background, they exhibit diminished CD4⁺ T cell development as compared with two other transgenic mouse lines carrying T cell receptors selected on I-A^b. T cells from mice exhibit uniformly high Vbeta6 expression and strong proliferative responses to human CLIP (hCLIP). These mice are useful in studies of T cell development and function.
005236	B6.Cg-Tg(TcraY1,TcrbY1)416Tev/J	Repository-Cryopreserved
	This transgenic strain carries a rearranged T cell receptor transgene specific for the H2-D^b-restricted SV40 large tumor antigen epitope I (residues 206-215). Flow cytometric analysis of lymphocytes detects approximately 94% of CD8+ T cells are specific for the tumor antigen. Mice that are homozygous for the transgenic insert are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of tumor immunology and peripheral T cell tolerance.
004338	B6;129-E2f2^tm1Zubi/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model ..... For more information please see the full descriiption on the strain data sheet
002121	B6;129P-Tcrb^tm1Mom Tcrd^tm1Mom/J	Repository-Cryopreserved
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
002117	B6;129P2-Tcrb^tm1Mom/J	Repository-Cryopreserved
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002119	B6;129P2-Tcrd^tm1Mom/J	Repository-Cryopreserved
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
002115	B6;129S2-Tcra^tm1Mom/J	Repository-Cryopreserved
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
004694	B6;D2-Tg(TcrLCMV)327Sdz/JDvsJ	Repository-Cryopreserved
	These mice carry a T-cell receptor (Tcra-V2, Tcra-J TA31 / Tcrb-V8.1, Tcrb-D, Tcrb-J 2.4) specific for LCMV (lymphocytic choriomeningitis virus), H2-D^b . They offer the unique possibility to examine T-cell tolerance to two independent antigens with the same transgenic mouse line. First, T-cell tolerance to LCMV has been studied in transgenic mice carrying the non-cytopathic LCM virus after neonatal infection. Second, the transgenic TCR use the beta-chain variable gene segment Tcrb-V8.1 that reacts preferentially with Mls^a (mixed lymphocyte stimulatory) antigen. Ten to twenty copies of the Tcr transgene are reportedly integrated on the same chromosome. The animals are on a mixed C57BL/6 and DBA/2 background but the MHC haplotype has been checked and found to be H2^b.
002408	B6;SJL-Tg(TcrAND)53Hed/J	Repository-Cryopreserved
	Mice express a T-cell receptor (V alpha 11.1 / V beta 3) specific for a carboxy-terminal fragment of pigeon cytochrome c and the E^k (class II MHC) molecule. Mice have been backcrossed a limited number of generations to C57BL/6 and fixed for H2^b. Since C57BL/6 lacks the E^k allele, this mouse must be crossed to a strain that expresses E^k to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. When crossed with a strain carrying E^k, F1 progeny express an abnormally high percentage of class II MHC restricted mature CD4+CD8- cells. The peripheral T-cell population is almost exclusively CD4+. The lack of expression of E^k in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing E^k .
004364	C.Cg-Tcra^tm1Mom Tcrb^tm1Mom/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable and fertile. Mutant mice display early stage arrest of alpha beta thymocyte differentiation. Mice may develop inflammatory bowel disease.
005533	C.Cg-Tg(Ins2-HA)165Bri/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control mice. Antibody titers of all transgenic mice tested were significantly higher than preimmune levels. Wh ..... For more information please see the full descriiption on the strain data sheet
002045	C.SJL-Tcra^c/SlkJ	Repository-Cryopreserved

002047	C.SJL-Tcrb^a Tcra^c/SlkJ	Repository-Cryopreserved

002046	C.SJL-Tcrb^a/SlkJ	Repository-Cryopreserved

003652	C57BL/6-Ptprcap^tm1Tho/J	Repository-Cryopreserved
	Homozygous knockout mice are viable and fertile and exhibit no gross defects. Thymocyte function and numbers appear normal, as do the percentages of CD4 and CD8 subsets. No gross abnormality in T- and B-cell antigen receptor signaling was detected.
003540	C57L/J-Tg(Tcrb)93Vbo/J	Repository-Cryopreserved
	This transgenic mouse was constructed with a rearranged genomic segment derived from the Tcrb locus. T lymphocytes express the transgenic TCRB chain on cell surfaces while the protein products encoded by endogenous Tcrb genes are not expressed. Homozygous mice generally don't survive beyond postnatal week four. This strain may provide a specific developmental marker for a prothymocyte lineage subset that lacks pluripotential properties.
005922	CBy.Cg-Thy1^a Tg(TcraCl1,TcrbCl1)1Shrm/J	Repository-Cryopreserved
	Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA_518-526) restricted by MHC class I H-2K^d. The phenotype below is as defined by the B10.D2 background (see Stock No. 005895). Flow cytometric analysis shows appropriate skewing towards the CD8⁺ T cell compartment in thymocytes and peripheral lymphocytes. CD8⁺ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1^a allele, rather than the alternate allele present in C57BL/10, DBA/2, ..... For more information please see the full descriiption on the strain data sheet
003448	CByJ.129P2(B6)-Tcrd^tm1Mom/Sz	Repository-Cryopreserved
	Mice homozygous for this targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4+CD8- and CD4-CD8+ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. 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 first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
005694	D1Lac.Cg-Tg(Tcra,Tcrb)24Efro/J	Repository-Cryopreserved
	Transgenic mice are viable, fertile, and normal in size. This mutant carries a transgene for a fully functional bovine and mouse type II collagen (260-267) specific IA^q-restricted T cell receptor. Flow cytometric analysis show 90% Tcrb-V8.3 expression of CD4+ splenocytes and greater than 95% expression in CD4+ lymphocytes. The transgene confers severe accelerated autoimmune arthritis following type II collagen (CII) immunization. Splenocytes from tolerized mice have altered activation and memory cell surface markers and high levels of Th2 cytokine secretion compared to control. Estradiol completely prevents collagen-induced arthritis (CIA). This mutant mouse may be useful in studies of CIA, rheumatoid arthritis, and T regulatory cells and may also serve as a source of T cells that mediate development of autoimmune diseases.
004673	NOD.129(B6)-Rag1^tm1Mom Cd80^tm1Shr/JbsJ	Repository-Cryopreserved
	The NOD.129(B6)Rag1^tm1MomCd80^tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1^tm1Mom and Cd80^tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80^tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80^tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1^tm1MomCd80^tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation.
004444	NOD.129P2(C)-Tcra^tm1Mjo/DoiJ	Repository-Cryopreserved
	NOD mice homozygous for the Tcra^tm1Mjo targeted mutation lack alpha beta T cells, and therefore, are completely protected from diabetes development. Because of the complete elimination of alpha beta T cells, these mice are useful in adoptive transfer experiments (as in Hoglund et al. 1999).
005513	NOD.129S2(B6)-Cd8a^tm1Mak/DvsJ	Repository-Cryopreserved
	Mice homozygote for the Cd8a^tm1Mak targeted mutation are deficient in functional cytotoxic T-cells; however helper T-cell development and function is comparable to normal. NOD.129S2(B6)-Cd8a^tm1Mak/DvsJ mice are homozygous for linkage markers delineating all known Idd loci of NOD origin and strongly diabetes resistant (1/17 females diabetic by 30 weeks of age). Survival of allogeneic skin grafts in NOD.129S2(B6)-Cd8a^tm1Mak/DvsJ mice treated with an anti-Cd40 ligand specific mAb and donor specific transfusion (DST) is significantly shorter (MST=21days) than in B6.129S2-Cd8a^tm1Mak/J (MST=101days) and (NODXB6)F1-Cd8a^tm1Mak (MST=35days) mice. Homozygous mutant mice are strongly, but not completely diabetes resistant (<3% in females) and insulitis is strongly, but not completely repressed. This model is useful for sorting out the genetic mechanism(s) involved in transplant tolerance and for > ..... For more information please see the full descriiption on the strain data sheet
004644	NOD.Cg Prkdc^scid-Tg(CSF2)2Ygy Tg(IL3)1Ygy Tg(KITLG)3Ygy/YgyJ	Repository-Cryopreserved
	Tg(IL3)1Ygy, Tg(CSF2)2Ygy, and Tg(KITLG)3Ygy encode porcine interleukin 3 (IL3), Porcine granulocyte macrophage-colony stimulating factor (CSF2, commonly designated GM-CSF) and soluble Porcine stem cell factor (KITLG, commonly designated sSCF) respectively. All three are individually driven by the human cytomegalovirus promoter. These three transgenes were co-injected and they co-segregate. RT-PCR detects transgenic expression of porcine IL-3, CSF2 and KITLG in bone marrow and spleen in NOD.Cg Prkdc^scid-Tg(IL3)1Ygy Tg(CSF2)2Ygy Tg(KITLG)3Ygy mice. Porcine IL3, CSF2, and KITLG are present in the serum of these mice in levels that can be detected by ELISA. NOD.Cg Prkdc ^scid-Tg(IL3)1Ygy Tg(CSF2)2Ygy Tg(KITLG)3Ygy/YgyJ not only provide a system in which long-term porcine tissue and stem cell engraftment can be achieved (Abe et al, 2002) but also is a useful tool for evaluating donor-specific tolerance induction by mixed chimerism across xenogeneic ba ..... For more information please see the full descriiption on the strain data sheet
006436	NOD.Cg-(Gpi1-D7Mit346)^C57BL/6J Tg(TcraAI4)1Dvs/DvsJ	Repository-Cryopreserved

006437	NOD.Cg-(Gpi1-D7Mit346)^C57BL/6J Tg(TcrbAI4)1Dvs/DvsJ	Repository-Cryopreserved

004347	NOD.Cg-Rag1^tm1Mom Tg(TcraAI4)1Dvs/DvsJ	Repository-Cryopreserved
	The rearranged Tcra transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1^tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcrbAI4)1DvsRag1^tm1Mom/DvsJ (004348), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile.
004348	NOD.Cg-Rag1^tm1Mom Tg(TcrbAI4)1Dvs/DvsJ	Repository-Cryopreserved
	The rearranged Tcrb transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1^tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcraAI4)1Dvs-Rag1^tm1Mom/DvsJ (004347), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile.
005273	NOD.Cg-Rag1^tm1Mom Cd86^tm2Shr Cd80^tm1Shr/JbsJ	Repository-Cryopreserved
	Mice homozygous for the Cd80^tm1Shr and Cd86^tm2Shr mutations are deficient in both CD80 and CD86. NOD mice defiecient for CD80, CD86 and Rag1 are viable and fertile, fail to produce T or B cells, and exhibit no signs of diabetes due to the absence of lymphocytes. In an immunocompetent NOD background, the Cd86^tm2Shr and Cd80^tm1Shr mutations exacerbate diabetes onset as well as a variety of other autoimmune diseases including thyroiditis, sialitis, exocrine pancreas disease and neuropathy when compared to normal NOD controls. These mice have also been observed, by the donating investigator, to be Treg-deficient. NOD.129(B6)-Rag1^tm1Mom Cd86^tm2ShrCd80^tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation and Treg function as they relate to autoimmune diseases and organ transplantation.
006024	NOD.Cg-Rag1^tm1Mom H2-Ab1^tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ	Repository-Cryopreserved
	Rag1 and H2-Ab1 deficient NOD mice carrying transgenes encoding humanized CD4 and HLA-DQ6 lack T and B cells and are free of autoimmune diabetes and cardiomyopathy, and do not develop thyroiditis. This model is useful in adoptive transfer experiments and in studying MHC class II-based resistance and susceptibility in autoimmunity.
006022	NOD.Cg-Rag1^tm1Mom H2-Ab1^tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ	Repository-Cryopreserved
	Rag1 and H2-Ab1 deficient NOD mice carrying transgenes coding for human CD2-CD4 and HLA-DQ8 lack T and B cells, and are diabetes free. Also, unlike the H2-Ab1 deficient, transgenic CD4, HLA-DQ8 mice (see Stock No. 006621), this strain does not develop cardiomyopathy. This model is useful in adoptive transfer experiments and to understand the role of MHC class II in autoimmunity.
005686	NOD.Cg-Thy1^a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Repository-Cryopreserved
	Transgenic mice, commonly referred to as NOD.clone-4 TCR, are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-K^d. FACS analysis of pancreatic lymph node indicates CFSE treated NOD clone-4 T cells adoptively transferred into NOD.InsHA (Stock No. 005685) proliferate vigorously and there is a 2-3-fold increase in the percentage of dividing clone-4 TCR, CD8⁺ T cells when compared to BALB/cBy (Stock Nos. 005307 and 005533) or B10.D2 (Stock Nos. 005308 and 005534). HA specific reactivity not tolerance is observed. This mouse is further modified with the Thy1^a allele, rather than the alternate allele Thy1^b present in C57BL/10, DBA/2, BALB/c and NOD/Lt mice. Thus, cell populations derived from these transgenic mice c ..... For more information please see the full descriiption on the strain data sheet
005685	NOD.Cg-Tg(Ins2-HA)165Bri/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The diabetes rate in transgenic females is similar to NOD females. FACS analysis using anti-HA antibodies indicates similar levels of HA expression on pancreatic beta cells as BALB-InsHA (Stock No. 005533). Tetramer (K^dHA) binding and dose titration analysis indicate CD8⁺ T cells obtained from transgenic mice exhibit high avidity for HA. Irradiated transgenic females adoptively transferred with transgenic CTL's exhibit rapid diabetes onset, whereas irradiated, non-transgenic NOD females do not become diabetic indicating HA antigen specificity. This model is useful for studying CD8⁺ T cell peripheral tolerance deficiency *(Kreuwel et al. 2001)*.
004696	NOD.Cg-Tg(TcrLCMV)327Sdz/DvsJ	Repository-Cryopreserved

006303	NOD.FVB-Tg(TcraBDC12-4.1)10Jos/GseJ	Repository-Cryopreserved
	This transgenic strain carries a rearranged Tcr alpha gene from the pathogenic anti-insulin CD4⁺ T-cell clone BDC12-4.1. Transgenic mice are viable and fertile. When hemizygotes are crossed with Stock No. 006304 NOD.FVB-Tg(TcrbBDC12-4.1)82Gse/GseJ, expression of the BDC12-4.1 T-cell receptor is confirmed by FACS analysis of PBMCs from the double transgenic mice. Double transgenic mice develop insulitis, but spontaneous diabetes does not develop, even in older animals (60 weeks of age), nor can insulin autoantibodies be detected in any age group. Splenocytes from double transgenic mice stimulated with B9-23 peptide produce IFN-gamma, whereas no response is observed in controls. When the congenic NOD double transgenic is combined with a homozygous Rag1^tm1Mom mutation (such as in Stock No. 003729), recombination of the endogenous TCR and immunoglobul ..... For more information please see the full descriiption on the strain data sheet
006304	NOD.FVB-Tg(TcrbBDC12-4.1)82Gse/GseJ	Repository-Cryopreserved
	This transgenic strain carries a rearranged Tcr beta gene from the pathogenic anti-insulin CD4⁺ T-cell clone BDC12-4.1. Transgenic mice are viable and fertile. When hemizygotes are crossed with Stock No. 006303 - NOD.FVB-Tg(TcraBDC12-4.1)10Jos/GseJ, expression of the BDC12-4.1 T-cell receptor is confirmed by FACS analysis of PBMCs from the double transgenic mice. Double transgenic mice develop insulitis but spontaneous diabetes does not develop, even in older animals (60 weeks of age), nor can insulin autoantibodies be detected in any age group. Splenocytes from double transgenic mice stimulated with B9-23 peptide produce IFN-gamma, whereas no response is observd in controls. When the congenic NOD double transgenic is combined with a homozygous Rag1^tm1Mom mutation (such as in Stock No. 003729), recombination of the endogenous TCR and immunoglobuli ..... For more information please see the full descriiption on the strain data sheet
005707	STOCK Rag1^tm1Mom Tg(TIE2-lacZ)182Sato/J	Repository-Cryopreserved
	Mice homozygous for both the targeted mutation and the transgene are viable and fertile. The transgene beta-galactosidase is well expressed, reflects endogenous Tek/Tie2 activity, and is specific to the vascular endothelium. Mice homozygous for the Rag1 mutation are immunodeficient as they lack mature B and T lymphocytes. This double mutant mouse may be useful in studies of cancer, tumor-related angiogenesis, and as a recipient of xenografted tumors.
002506	STOCK Tg(CD3E)26Cpt-Rag1^tm1Mom/J	Repository-Cryopreserved
	Mice carrying both the (CD3E)26Cpt transgene (Stock No. 002194) and the Rag1^tm1Mom targeted mutation exhibits characteristics of both mutant strains. Double homozygous mutant mice produce no mature T, B, or NK cells. They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage.
002597	STOCK Tg(TcrHEL3A9)1Mmd/J	Repository-Cryopreserved
	Mice carrying the (TcrHEL3A9) transgene express the alpha and beta chains of a T-cell receptor specific for hen egg lysozyme. Transgenics are used to study maintenance and breakdown of immunological tolerance, overcoming of the anergic state, and issues of costimuli.

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Strains from the Research Colonies of Jackson Laboratory Scientists

IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.

Stock Number	Strain Name Strain Description	Standard Supply
004257	NOD.Cg-Prkdc^scid Tg(TcrLCMV)327Sdz/Dvs	Research Strain
	These mice do not develop diabetes; The presence of the T cell receptor expressing transgene does not alter the resistance to type 1 diabetes conferred to the NOD background by homozygosity for the scid mutation.
004259	NOD.Cg-Rag1^tm1Mom Tg(TcraAI4)1Dvs/+ Tg(TcrbAI4)1Dvs/+	Research Strain

004334	NOD/ShiLt-Tg(TcraAI4)1Dvs	Research Strain

003868	NOD/ShiLt-Tg(TcraAI4)1Dvs/+ Tg(TcrbAI4)1Dvs/+	Research Strain

004335	NOD/ShiLt-Tg(TcrbAI4)1Dvs	Research Strain

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New Strains Under Development

(See informational text following listing of strains)

How to Register Interest
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 New Strains Under Development
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
006775	NOD.Cg-Foxp3^sf/DoiJ	On Hold
Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development.
007962	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J	Under Development for Production
These compound transgenic mice carry a rat Erbb2/HER-2/neu oncogene tagged with ovalbumin epitopes OT-I and OT-II, which are recognized by T cell receptors, under the control of the MMTV promoter (termed fusion protein neu^OT-I/OT-II). In addition, this strain carries a mouse Trp53 mini-gene, harboring a G to A point mutation in codon 172 (changing Arg to His; R172H) driven by the rat whey acidic protein promoter. Approximately 85% of compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age. This strain may be useful in studies of cancer immunotherapy.
008074	C.129S4-Traf1^tm1Tsi/TsiPryhJ	Under Development for Production
Mice homozygous for the TRAF1 mutant allele (TRAF1^-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1^-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1^-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that elicit enhanced Th2 responses in vivo. BALB/c-TRAF1^-/- T cells exhibit elevated nuclear expression of NFAT-interacting protein (NIP45) and also induce significantly more intense pulmonary inflammation and higher airway hyper-responsiveness in OVA allergic inflammation models. Pulmonary leukocyte recruitment is attenuated following inhalation of lipopolysaccharide in BALB/c-TRAF1^-/- mice. Homozygous mice on a C57BL/6 congenic background ( ..... For more information please see the full description on the strain data sheet
008309	C57BL/6-Rag2^tm1Cgn/J	Under Development for Production
Mice homozygous for the RAG-2^fl 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-2^fl 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.
003447	CBy.129P2(B6)-Tcrb^tm1Mom/SzJ	Under Development for Production
Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wild-type; CD4⁺CD8⁺ cells ~6% of wild-type. The proportion of CD4-CD8- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age. 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 first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessa ..... For more information please see the full description on the strain data sheet
007081	CByJ.129P2(B6)-Tcrb^tm1Mom/J	Under Development for Production

007082	CByJ.129S(B6)-Tnf^tm1Gkl/J	Under Development for Production
Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full description on the strain data sheet
007080	CByJ.B6-Tg(TcraTcrb)1100Mjb/J	Under Development for Production
These mice contain transgenic inserts for mouse Tcra-V2 and Tcrb-V5 genes. The transgenic T cell receptor was designed to recognize ovalbumin residues 257-264 in the context of H2K^b and used to study the role of peptides in positive selection and the response of CD8⁺ T cells to antigen. Like most TCR transgenics, these mice are somewhat immunodeficient. 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 first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008659	NOD.Cg-Rag1^tm1Mom Ins2^Akita Prf1^tm1Sdz/SzJ	Under Development for Production
Like NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/J (004848), this strain lacks mature T and B cells. NK cells, although present, lack cytotoxic activity. Both sexes develop spontaneous hyperglycemia as early as 3 weeks of age, however, the phenotype is predominantly exhibited by males. Pancreatic islets have reduced insulin staining and exhibit an altered morphology with age. Human islet transplantation at doses of 4000 IEQ is successful in returning hyperglycemic males to a euglycemic state. This strain may useful in studies of human islet and beta stem and progenitor cell function.

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New Strains Under Development
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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. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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