Mice homozygous for Il10tm1Cgn exhibit an Il10-deficiency which is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli, increased prevalence of colorectal adenocarcinoma and spontaneous development of chronic enterocolitis. . These IL-10 mutant mice may be useful studying inflammatory bowel disease (Crohn's disease and/or colitis), cancer, innate and adaptive immunity, and many other areas of inflammatory or autoimmunity research.
Donna Rennick, DNAX Research Institute
Genetic Background | Generation |
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000651 BALB/cJ |
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Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Il10 | interleukin 10 |
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, and many other areas of inflammatory or autoimmunity research.
The onset and severity of both spontaneous and experimentally-induced inflammatory phenotype of Il10-deficient mice is strongly influenced by the genetic background and the husbandry conditions (specific health status/commensal flora) of the vivaria in which mice are maintained.
For example, inflammatory bowel disease (IBD; colitis and Crohn's disease) severity in mouse models is dependent upon interactions between specific genetic background and environmental factors (an as yet undefined component of the enteric flora of which Helicobacter spp. appear to be associated, but not specifically the environmental trigger). Both spontaneous and induced models of IBD demonstrate that susceptibility to intestinal inflammation varies markedly among inbred strains of mice. Generally, for Il10-deficient models on defined genetic backgrounds, the severity of colitis-related characteristics is most severe on C3H/HeJBir (Stock No. 004326 and Stock No. 003968) or 129/Sv (Stock No. 004368), intermediate on BALB/cJ (Stock No. 004333) or NOD/Lt (Stock No. 004266), and least severe on C57BL/10 (Stock No. 002250) or C57BL/6J (Stock No. 002251). Furthermore, the husbandry conditions (specific health status/commensal flora) of the vivaria in which mice are maintained significantly alter the onset and severity of spontaneous IBD; higher SPF conditions are associated with attenuated colitis. Il10-deficient mice on both the C3H/HeJBir and C57BL/6J genetic backgrounds exhibit a significant increase in peripheral blood granulocyte populations upon lesion development and this metric may be used as a robust non-lethal assessment of Il10-deficiency induced colitis onset and severity. Other indications of Il10-deficiency induced colitic lesion onset may include perianal ulceration (C3H/HeJbir background) or rectal prolapse (C57BL/6J background).
The Il10tm1Cgn mutation was created by in the Laboratory of Dr. Werner Muller at the University of Cologne. Briefly, a targeting vector was designed to replace codons 5-55 of exon 1 of the targeted gene with a 24 bp linker (providing a termination codon) and a neo expression cassette, as well as introduce a termination codon into exon 3. The construct was electroporated into 129P2/OlaHsd-derived E14-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient C57BL/6 blastocysts and chimeric males were bred with C57BL/6 females to establish the mutant colony on a mixed B6;129P2 genetic background. Subsequently, mutant mice were backcrossed to the BALB/c genetic background for several generations to generate this strain. Simple sequence length polymorphism (SSLP) analysis confirmed that there are no chromosomal segments derived from 129 or C57BL/6, except for regions immediately flanking the disrupted locus.
Allele Name | targeted mutation 1, University of Cologne |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | IL-10-; Il10-; IL-10 KO; IL-10KO; Il10tmCgn; IL-10KO |
Gene Symbol and Name | Il10, interleukin 10 |
Gene Synonym(s) | |
Strain of Origin | 129P2/OlaHsd |
Chromosome | 1 |
Molecular Note | A 500 bp genomic fragment containing codons 5-55 was replaced with a linker containing a termination codon followed by a neomycin cassette. A termination codon was also introduced into exon 3. No IL10 activity was detectable by ELISA assays in supernatants of in vitro cultures of Con A-stimulated splenic T cells derived from homozygous mice following infection with the nematode N. brasiliensis. |
Mutations Made By | Dr. Ralf Kuhn, Max-Delbrück Center for Molecular Medicine |
This strain originated on a B6;129P2 background and has been backcrossed for 18 generations on the BALB/cJ (Stock No. 000651) background. When maintaining a live colony, homozygous mice may be bred together. As homozygous mice are more susceptible to pathogenic bacteria, high specific pathogen-free (SPF) conditions are recommended for optimal breeding. However, the onset and severity of both the spontaneous and experimentally-induced inflammatory phenotype of Il10-deficient mice is strongly influenced by the genetic background and the husbandry conditions (specific health status/commensal flora) of the vivaria in which mice are maintained and such high SPF conditions may attenuate the desired Il10-deficient phenotype.
When using the BALB IL-10 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #004333 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Heterozygous for Il10<tm1Cgn> |
Frozen Mouse Embryo | C.129P2(B6)-Il10<tm1Cgn>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | C.129P2(B6)-Il10<tm1Cgn>/J Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | C.129P2(B6)-Il10<tm1Cgn>/J Frozen Embryos | $3373.50 |
Frozen Mouse Embryo | C.129P2(B6)-Il10<tm1Cgn>/J Frozen Embryos | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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