Search Criteria: Research Area is "Hematological Research: Anemia, Iron Deficiency and Transport Defects (hemolytic)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002251 | B6.129P2-Il10tm1Cgn/J | 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 | ||
| 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 | ||
| 004368 | 129(B6)-Il10tm1Cgn/J | Repository- Live |
| 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 | ||
| 002250 | B10.129P2(B6)-Il10tm1Cgn/J | Repository- Live |
| 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 | ||
| 002252 | B6.129P2-Il2tm1Hor/J | Repository- Live |
| Homozygous mutant mice show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wild-type. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between six and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die three to five weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the
..... For more information please see the full descriiption on the strain data sheet | ||
| 004333 | C.129P2(B6)-Il10tm1Cgn/J | Repository- Live |
| 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 | ||
| 005912 | B6.Cg-Il10tm1Cgn (D3Mit49-D3Mit348)/Lt | Repository-Cryopreserved |
| Homozygous mice are IL10-deficient and develop spontaneous colitic lesions in the cecum and large intestine as early as 6-8 weeks of age. The severity and age of onset of colitis varies with the donor type and location of the cytokine deficiency colitis susceptibility 1 (Cdcs1) interval. Generally, the C3H/HeJBir region encompassed by D3Mit348 through D3Mit254 (127.7-132.5 megabases) confers increased colitis susceptibility on the B6.129P2-Il10tm1Cgn background (Beckwith J, et al., 2005). Mice on the B6.129P2-Il10tm1Cgn background are prone to rectal prolapse particularly when carrying susceptibility alleles from Chromosome 3. Granulocyte populations in peripheral blood increase upon lesion development and provide a robust non-lethal assessment of colitis severity. | ||
| 002229 | C.129P2(B6)-Il2tm1Hor/J | Repository-Cryopreserved |
| Homozygous mutant mice for the Il2tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de
..... For more information please see the full descriiption on the strain data sheet | ||
| 002228 | C3.129P2(B6)-Il2tm1Hor/J | Repository-Cryopreserved |
| Homozygous mutant mice for the Il2tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de
..... For more information please see the full descriiption on the strain data sheet | ||
| 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 | ||
| 002573 | NOD.129P2(B6)-Il2tm1Hor/DvsJ | Repository-Cryopreserved |
| 005346 | NOD.Cg-Il10tm1Cgn Casp1tm1Sesh/LtJ | Repository-Cryopreserved |
| Mice homozygous for the Il10 and Casp1 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 strains. The Il10 targeted 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. | ||
| 004291 | NOD.Cg-Il10tm1Cgn Il4tm1Cgn/DvsJ | Repository-Cryopreserved |
| 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. | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Repository-Cryopreserved |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt 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. | ||
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