| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002253 | B6.129P2-Il4tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. | ||
| 002496 | BALB/c-Il4tm2Nnt/J | Repository- Live |
| Mice homozygous for the Il4tm2Nnt targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. Susceptible to infection by Leishmania major despite deficiency in IL4. | ||
| 004190 | C.129-Il4tm1Lky/J | Repository- Live |
| Mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knockin replaces the endogenous gene with an Il4/IRES/EGFP gene (IL4 activity remains intact). This leads to generation of a bicistronic transcript under the control of endogenous regulatory elements. Cells activated to express IL4 will express EGFP, allowing reliable in vivo tracking of both innate and adaptive immune cells, and/or enabling their isolation without further stimulation. As the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice can also be used to report competence for IL4 production upon stimulation. | ||
| 002518 | C57BL/6-Il4tm1Nnt/J | Repository- Live |
| Mice homozygous for the Il4tm1Nnt targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. | ||
| 002574 | NOD.129P2(B6)-Il4tm1Cgn/Dvs | Research Strain |
| 003480 | C.129S2(B6)-Il4tm1Gru/J | Cryopreserved - Ready for recovery |
| This strain was made using gene targeting in embryonic stem cells to modify the Il4 locus by knocking-in a transmembrane domain. Expression of Il4 in a membrane-bound form provides a novel method for the identification and characterization of Il4-producing cells. | ||
| 002230 | C57BL/6J-Tg(LckIl4)1315Dbl/J | Cryopreserved - Ready for recovery |
| Transgenic mice overexpressing the IL4 transgene under the control of the Lck promoter show severe osteoporosis of both cortical and trabecular bone by 2 months in both males and females. There is decreased bone formation by osteoblasts and kyphosis; characterized by long snout ("weasel face") by 6 weeks of age. | ||
| 005879 | D1Lac.Cg-Il4tm1Cgn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene product is detectable in splenocyte supernatants. Mutant mice crossed to the DBA/1LacJ background (I-Aq haplotype) are susceptible to collagen-induced arthritis. Deletion of the endogenous gene exacerbates both the incidence and severity of collagen-induced arthritis, which is accompanied with increased IgG2 and decreased IgG1 in sera. Following type II collagen (CII) tolerization of mutant mice, splenocytes cultured with CII have increased Th2 (IL-5, IL-9, IL-10, IL-13) and Th1 (IFNgamma, IL-6) cytokines. Mutant mice may be useful in other studies of collagen-induced arthritis, rheumatoid arthritis, mechanisms of tolerance, regulation of autoimmune disease, and T helper cell immune responses. On the C57BL/6 background (see Stock No. 002253) from which this mouse was created, T and B cell development is nor ..... | ||
| 004222 | NOD.129P2(B6)-Il4tm1Cgn/DvsJ | Cryopreserved - Ready for recovery |
| Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001) | ||
| 004291 | NOD.Cg-Il10tm1Cgn Il4tm1Cgn/DvsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10 and Il4 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 006698 | NOD.Cg-Il4tm1Lky/JbsJ | Cryopreserved - Ready for recovery |
| A "knock-in" replaces the endogenous gene with an Il4/IRES/EGFP bicistronic construct, which places both IL4 and EGFP expression under the control of the endogenous Il4 gene regulatory elements. IL4 activity in these mutant mice remains intact. Cells activated to express IL4 also express EGFP allowing reliable in vivo tracking of both innate and adaptive immune cells and enabling their isolation without further stimulation. Because the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice also can be used to report competence for IL4 production upon stimulation. This knock-in allele has been backcrossed to NOD for 15 generations. Diabetes incidence in mutant mice is reported to be about 60%, which is not statistically different from wild-type cohorts or NOD inbred mice. | ||
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