Search Criteria: Research Area is "Immunology and Inflammation Research: Inflammation (rheumatoid arthritis)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000482 | B6.MRL-Faslpr/J | Level 3 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full descriiption on the strain data sheet | ||
| 000485 | MRL/MpJ-Faslpr/J | Level 4 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-lpr/lpr mouse but not the MRL normal (Hewicker 1990). Onset and severity of symptoms associated with the Faslpr gene is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr
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..... For more information please see the full descriiption on the strain data sheet | ||
| 000480 | C3.MRL-Faslpr/J | Repository- Live |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full descriiption on the strain data sheet | ||
| 006825 | MRL/MpJ-Faslpr/2J | Repository- Live |
| The current colony (as of fall 2006) of MRL/MpJ-Faslpr/J has experienced a progressive loss of lymphoproliferative phenotype over the past several years, as reported by some of our customers and as observed by our technical staff. This loss of phenotype has been manifested by reduced enlargement of brachial and mesenteric lymph nodes, and poor splenomegaly. Also, the life spans of the mice in the current colony have also been found to be much longer than the historically observed and reported 17 weeks for females and 22 weeks for males. However, genotyping continues to show that all the mice in the colony remain homozygous for the Faslpr mutation, and the SNP profile in the region of the mutation on Chromosome 19 has not changed.
In an effort to regenerate the desired phenotype, we recovered mice from our embryo archive cryopreserved in 1993. The sixteen-week old cryo-recovered mice have lymph nodes that were 4.5 (females) to 10.1 times (male) la
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| 005879 | D1Lac.Cg-Il4tm1Cgn/J | Repository-Cryopreserved |
| 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
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| 005705 | FVB-Tg(KRT14-Vegfa)3Dtm/J | Repository-Cryopreserved |
| Mice hemizygous for the transgene are viable and fertile. Transgene expression is demonstrated in the basal keratinocyte layer of the epidermis and outer root sheath keratinocytes of hair follicles. Homozygous mice spontaneously develop severe psoriasis-like lesions between 3-6 months of age, where hemizygous mice do not. Transgenic mice have increased density of tortuous cutaneous blood capillaries with elevated expression of select VEGF receptors, most prominently in neonates. Dermal mast cell localization and capillary hyperpermeability are also increased. Postcapillary venules exhibit significantly enhanced leukocyte rolling and adhesion. Transgenic expression promotes lymphangiogenesis associated not only with delayed-type hypersensitivity induced psoriasis-like skin inflammation but also with cutaneous tissue repair after wounding. Further, transgenic mice have accelerated chemically induced skin carcinogenesis with tumor associated lymphangiogenesis and angiogenesis. Elevated me
..... For more information please see the full descriiption on the strain data sheet | ||
| 002455 | MRL-Faslpr.129P2(B6)-B2mtm1Unc | Repository-Cryopreserved |
| Mice homozygous for both the lymphoproliferation spontaneous mutation (Faslpr) and the B2mtm1Unc targeted mutation are viable and fertile. Class I molecule-deficient B2mtm1Unc mice were backcrossed to MRL/MpJ-Faslpr to study the role of MHC class I molecules in the development of systemic autoimmune disease. Double homozygous mutant mice demonstrated a substantial reduction in CD4-CD8- T cells and a diminution of autoimmune disease. Specifically, hypergammaglobulinemia; autoantibodies including anti-DNA, anti-Smith antigen, and rheumatoid factor; and glomerulonephritis were significantly reduced compared to MRL/MpJ-Faslpr homozygous mice. Moreover, the pattern of hypergammaglobulinemia suggests that the requirement for MHC class I proteins is restricted temporally to later stages of the disease. | ||
| 003896 | MRL/MpJ Faslpr-Foxq1sa-J/J | Repository-Cryopreserved |
| MRL/MpJ, and one of its ancestral strains LG/J, display heightened wound healing relative to a panel of other inbred strains. At 4 weeks post-injury, 2mm ear punch wounds healed to 0-0.4mm in MRL/MpJ mice but were still 1.2-1.6mm in C57BL/6 mice. At 15 days post-injury C57BL/6 showed a maximal closure of 30% reduction in ear hole size while MRL showed 85% reduction. The process of healing in MRL/MpJ mice was faster, more complete, showed increased swelling, angiogenesis, fibroblast migration, extracellular matrix deposition, and decreased scarring and fibrosis. Additionally, hair follicles and accompanying sebaceous glands were regenerated to a much greater degree. The other ancestral strains of MRL/MpJ (C3H, C57BL/6, and AKR) do not display this enhanced healing. Bone marrow transplantation showed that the MRL/MpJ healing phenotype did not readily transfer with bone marrow and did remain in the irradiated host tissues. Enhanced healing of cardiac wounds has also been reported in MRL/M
..... For more information please see the full descriiption on the strain data sheet | ||
| 004519 | NOD.MRL(C3)-Faslpr/DoiJ | Repository-Cryopreserved |
| NOD mice homozygous for the Tnfrsf6 lpr mutation are deficient in Fas antigen expressed on cell surfaces, and the disruption of the Fas-mediated apoptotic pathway results in severe lymphoma in NOD by 4 months of age. This lymphoma is characterized by an expansion of unusual CD4 -, CD8 -, CD3 low , B220 + lymphocytes. Forty week-old NOD mice homozygous for the Tnfrsf6 lpr mutation are completely protected from spontaneous diabetes and insulitis (as compared to 68% diabetes incidence in the control NOD), even after adoptive transfer of lymphocytes from diabetic NOD mice (0% diabetes incidence 12 weeks post transfer, as compared to NOD controls with 85% incidence 12 weeks post transfer). Recent evidence indicates that Fas-deficient NOD mice are resistant to the adoptive transfer because the abnormal subset of CD4 -, CD8 -, CD3 low , B220 + lymphocytes ..... For more information please see the full descriiption on the strain data sheet | ||
| 004922 | NOD.MRL-Faslpr/Dvs | Repository-Cryopreserved |
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