Search Criteria: Research Area is "Immunology and Inflammation Research: CD Antigens, Antigen Receptors, and Histocompatibility Markers (Tlr deficiency)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066
..... For more information please see the full descriiption on the strain data sheet | ||
| 004326 | C3Bir.129P2(B6)-Il10tm1Cgn/Lt | Level 3 |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a
..... For more information please see the full descriiption on the strain data sheet | ||
| 004650 | B6.129-Tlr2tm1Kir/J | Level 4 |
| 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 isolated peritoneal macrophages. Bone marrow derived macrophages do not respond to spirochete (Borrelia burgdorferi) lipoprotein challenge, although non-lipoprotein sonicate stimulates activation. Arthritis due to B. burgdorferi infection, as assessed by rear ankle swelling, is more severe in mutant mice. Tissues of infected mutants can contain up to 100 times higher bacteria levels than those found in wildtype littermates. Elevated spirochete numbers persist 8 weeks post-infection. Homozygotes do not produce TNF-alpha or IL-6, and do not develop symptoms of illness when treated with leptospiral (Leptospira interrogans) lippolysaccharide (LPS). This mutant mouse strain may be useful in studies of host response to bacterial endotoxins such as septic shock. | ||
| 002930 | C.C3-Tlr4Lps-d/J | Level 4 |
| In addition to the Tlr4Lps-d congenic interval from C3H/HeJ, this strain is also congenic for the wild type tyrosinase allele from C3H/HeJ on chromosome 7. This strain provides a tool for analysis of markers in the region and for examining functional effects of Lpsd on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors. | ||
| 007227 | B6.B10ScN-Tlr4lps-del/JthJ | Repository- Live |
| This spontaneous mutation is a 7 kb deletion in the Tlr4 gene, which results in absence of both mRNA and protein and thus exhibits a defective response to LPS stimulation. The functionally similar Tlr4Lps-d mutation found in C3H/HeJ mice is a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4lps-n, occurs in most other C3H and C57BL/10 substrains and most mouse strains. This strain may be used to study the Toll signalling pathway and susceptibility to Gram-negative bacterial infection. | ||
| 005217 | B6;129S1-Tlr3tm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis detects a truncated gene product (mRNA), which is not functional. Unlike wildtype macrophages, macrophages derived from these animals fail to produce inflammatory cytokines, IFN-alpha or IFN-beta when challenged with poly(I:C), polyinosine-polycytidylic acid, a synthetic dsRNA analog. Splenocytes isolated from homozygotes do not respond to viral dsRNA and have diminished IL-6 production. Mice homozygous for the mutation are resistant to poly(I:C) induced shock and produce lower levels of IL-12. This mutant mouse strain may be useful in studies of the toll-like receptor pathway of innate immune response. | ||
| 003752 | C57BL/10ScNJ | Repository- Live |
| The breeder pair of C57BL/10ScN mice, obtained from NIH, that were the progenitors of all mice of this strain at The Jackson Laboratory were tested by PCR analysis for the spontaneous Il12rb2 mutation described by Poltorak et al. (J. Immunol. 167:2106-2111, 2001) and found to carry only the wild type Il12rb2 allele. C57BL/10ScN mice have a deletion of the Tlr4 gene that results in absence of both mRNA and protein and thus in defective response to LPS stimulation. Tlr4lps-del differs from the Tlr4Lps-d mutation of C3H/HeJ mice, a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4lps-n, occurs in most other C3H and C57BL/10 substrains and most other mouse strains. | ||
| 005973 | C3Bir.129P2(B6)-Il10C3Bir/LtJ | Repository-Cryopreserved |
| This is a control strain for C3Bir.129P2(B6)-Il10tm1Cgn/Lt (Stock No. 004326), developed in parallel with the latter until backcrossing was complete. As such, it does not exhibit the Il10-deficient phenotype. | ||
| 003968 | C3Bir.129P2(B6)-Il10tm1Cgn/LtJ | Repository-Cryopreserved |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a
..... For more information please see the full descriiption on the strain data sheet | ||
| 005972 | C3H/HeJBirLtJ | Repository-Cryopreserved |
| Under conventional housing conditions, C3H/HeJBirLtJ mice develop spontaneous colitis. It should be noted that the phenotype of cecocolitis in this strain requires an interaction with an as yet undefined component of the enteric flora. Inflammation is present mainly in the cecum and right colon. Colitis develops early in life and resolves by three months of age. The colitis is characterized by acute and chronic inflammation, ulcerations, crypt abscesses, regenerative hyperplasia and submucosal scarring. A mild recurrence of the disease can occur after one year. Small lesions at the anorectal junction are common throughout life. | ||
(10 stocks) Back to Top
Send questions to our Technical Support team using the Express Technical Support Form.
(3.2)