Strain Name:

C3Bir.129P2(B6)-Il10tm1Cgn/LtJ

Stock Number:

003968

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Availability:

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names C3Bir.129P2(B6)-Il10tm1Cgn/J    (Changed: 14-DEC-05 )
Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
 
Donating InvestigatorDr. Edward Leiter,   The Jackson Laboratory

Description
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).

For a more detailed description please refer to the JAX Notes Fall 1997 article.

Development
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 C3H/HeJBir genetic background for at least 12 generations to generate this strain.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying   Il10tm1Cgn     (10 strains)

Strains carrying   Pde6brd1 allele
004202   B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J
000002   B6.C3-Pde6brd1 Hps4le/J
001022   B6C3FeF1/J a/a
000652   BDP/J
000653   BUB/BnJ
002439   C3.129P2(B6)-B2mtm1Unc/J
005494   C3.129S1(B6)-Grm1rcw/J
000509   C3.Cg-Lystbg-2J/J
000480   C3.MRL-Faslpr/J
001957   C3A Pde6brd1.O20/A-Prph2Rd2/J
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
006435   C3Fe.SW-Soaa/MonJ
001904   C3H-Atcayji-hes/J
000659   C3H/HeJ
000511   C3H/HeJ-Ap3d1mh-2J/J
000784   C3H/HeJ-Faslgld/J
002433   C3H/HeJ-Sptbn4qv-lnd2J/J
005972   C3H/HeJBirLtJ
001824   C3H/HeJSxJ
000635   C3H/HeOuJ
000474   C3H/HeSn
001431   C3H/HeSn-ocd/J
000661   C3H/HeSnJ
002333   C3H/HeSnJ-gri/J
001576   C3He-Atp7btx-J/J
000658   C3HeB/FeJ
002588   C3HeB/FeJ-Eya1bor/J
001533   C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J
001908   C3HfB/BiJ
001502   C3Sn.B6-Epha4rb/EiGrsrJ
002235   C3Sn.C3-Ctnna2cdf/J
001547   C3Sn.Cg-Cm/J
001906   C3fBAnl.Cg-Catb/AnlJ
000656   CBA/J
000813   CBA/J-Atp7aMo-pew/J
000660   DA/HuSnJ
000023   FL/1ReJ
000025   FL/4ReJ
003024   FVB.129P2(B6)-Fmr1tm1Cgr/J
002539   FVB.129P2-Abcb4tm1Bor/J
002935   FVB.129S2(B6)-Ccnd1tm1Wbg/J
002953   FVB.Cg-Tg(MMTVTGFA)254Rjc/J
003170   FVB.Cg-Tg(Myh6-tTA)6Smbf/J
003078   FVB.Cg-Tg(WapIgf1)39Dlr/J
003487   FVB.Cg-Tg(XGFAP-lacZ)3Mes/J
003257   FVB/N-Tg(GFAPGFP)14Mes/J
002856   FVB/N-Tg(TIE2-lacZ)182Sato/J
002384   FVB/N-Tg(UcpDta)1Kz/J
001800   FVB/NJ
001491   FVB/NMob
000804   HPG/BmJ
000734   MOLD/RkJ
000550   MOLF/EiJ
002423   NON/ShiLtJ
000679   P/J
000680   PL/J
000268   RSV/LeJ
000269   SB/LeJ
010968   SB;C3Sn-Lrp4mdig-2J/GrsrJ
005651   SJL.AK-Thy1a/TseJ
000686   SJL/J
000688   ST/bJ
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
002648   STOCK a/a Cln6nclf/J
000279   STOCK gr +/+ Ap3d1mh/J
005965   STOCK Tg(Pomc1-cre)16Lowl/J
004770   SW.B6-Soab/J
002023   SWR.M-Emv21 Emv22/J
000689   SWR/J
000939   SWR/J-Clcn1adr-mto/J
000692   WB/ReJ KitW/J
100410   WBB6F1/J-KitW/KitW-v/J
000693   WC/ReJ KitlSl/J
View Strains carrying   Pde6brd1     (73 strains)

Strains carrying   Tlr4Lps-d allele
002930   C.C3-Tlr4Lps-d/J
005973   C3Bir.129P2(B6)-Il10C3Bir/LtJ
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
000659   C3H/HeJ
005972   C3H/HeJBirLtJ
View Strains carrying   Tlr4Lps-d     (5 strains)

Strains carrying other alleles of Il10
014530   B6(Cg)-Il10tm1.1Karp/J
008379   B6.129S6-Il10tm1Flv/J
005973   C3Bir.129P2(B6)-Il10C3Bir/LtJ
View Strains carrying other alleles of Il10     (3 strains)

View Strains carrying other alleles of Pde6b     (13 strains)

Strains carrying other alleles of Tlr4
024872   B6(Cg)-Tlr4tm1.1Karp/J
007227   B6.B10ScN-Tlr4lps-del/JthJ
000029   BXD29-Tlr4lps-2J/J
003752   C57BL/10ScNJ
View Strains carrying other alleles of Tlr4     (4 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Inflammatory Bowel Disease 23; IBD23
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Graft-Versus-Host Disease, Susceptibility To; GVHDS   (IL10)
Human Immunodeficiency Virus Type 1, Susceptibility to   (IL10)
Rheumatoid Arthritis; RA   (IL10)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Il10tm1Cgn/Il10tm1Cgn

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • premature death
    • ~30% of homozygotes succumb to disease within 3 months of age   (MGI Ref ID J:15222)
    • death is correlated with anemia and gradual weight loss   (MGI Ref ID J:15222)
    • at >3 months of age, mortality is increased but never reaches 100%   (MGI Ref ID J:15222)
  • digestive/alimentary phenotype
  • abnormal intestinal epithelium morphology   (MGI Ref ID J:15222)
    • abnormal enterocyte morphology   (MGI Ref ID J:15222)
    • abnormal intestinal mucosa morphology   (MGI Ref ID J:15222)
      • at 9 weeks, 59% of mice displaying colitis develop a high grade dysplasia of the colonic mucosa   (MGI Ref ID J:68476)
      • abnormal crypts of Lieberkuhn morphology   (MGI Ref ID J:15222)
  • abnormal large intestine morphology
    • minimal epithelial hyperplasia at 3 weeks   (MGI Ref ID J:35020)
    • prominent epithelial hyperplasia at 3 months   (MGI Ref ID J:35020)
    • abnormal colon morphology
      • colonic prolapse is observed in some older mutants   (MGI Ref ID J:107077)
  • intestinal inflammation   (MGI Ref ID J:35020)
    • anemic and underweight homozygotes display enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon   (MGI Ref ID J:15222)
    • inflammation was limited to the proximal colon under specific pathogen free conditions   (MGI Ref ID J:15222)
    • spontaneous inflammatory bowel disease (IBD) develops by 5 weeks in some animals   (MGI Ref ID J:107077)
    • large intestinal inflammation
      • lymphocytes and small numbers of neutrophiles as infiltrates in the lamina propria of the cecum, ascending and transverse colon at three weeks   (MGI Ref ID J:35020)
      • multifocal lesions in all regions of the large intestine at three months   (MGI Ref ID J:35020)
      • occasional transmural inflammation and crypt abscesses at 3 months   (MGI Ref ID J:35020)
      • more ulcerations at 6 months   (MGI Ref ID J:35020)
      • cecum inflammation   (MGI Ref ID J:35020)
      • colitis
        • all Il10-null mice develop colitis by the age of 9 weeks in contrast to wild-type littermates   (MGI Ref ID J:68476)
    • small intestinal inflammation
      • 8% with duodenitis at 3 months of age   (MGI Ref ID J:35020)
      • increased duodenitis at 6 months   (MGI Ref ID J:35020)
  • growth/size/body phenotype
  • cachexia
    • although some homozygotes with slow disease progression show normal body weights up to 12 weeks of age, all homozygotes are eventually affected by weight loss   (MGI Ref ID J:15222)
    • at 7-11 weeks of age, most homozygotes display a ~30% weight reduction relative to wild-type controls   (MGI Ref ID J:15222)
  • postnatal growth retardation
    • at 7-11 weeks of age, ~75% of homozygotes are growth retarded relative to wild-type controls   (MGI Ref ID J:15222)
    • growth retardation is first observed between 3 and 4 weeks of age   (MGI Ref ID J:15222)
  • hematopoietic system phenotype
  • abnormal leukocyte morphology   (MGI Ref ID J:35020)
    • abnormal lymphocyte cell number
      • double control levels in the lamina propria   (MGI Ref ID J:35020)
      • increased CD4-positive T cell number
        • elevated   (MGI Ref ID J:35020)
        • activated memory phenotype   (MGI Ref ID J:35020)
    • decreased T cell proliferation
      • reduced proliferative response of CD4+ cells to UVB irradiation   (MGI Ref ID J:125760)
    • increased granulocyte number
      • homozygotes display up to a 2-fold elevation in leukocyte numbers due to an increase in granulocytes   (MGI Ref ID J:15222)
      • elevated at 3 weeks and increasing with age   (MGI Ref ID J:35020)
  • abnormal level of surface class II molecules   (MGI Ref ID J:15222)
  • abnormal myelopoiesis
    • severely anemic homozygotes display a hyperproliferative myeloid compartment   (MGI Ref ID J:15222)
  • absent erythroid progenitor cell
    • severely anemic homozygotes show complete depletion of eythroid cells in the bone marrow   (MGI Ref ID J:15222)
  • anemia
    • at 7-11 weeks of age, ~90% of homozygotes exhibit anemia, most likely due to iron deficiency   (MGI Ref ID J:15222)
    • the observed anemia is most often defined as microcytic or normocytic and hypochromic   (MGI Ref ID J:15222)
    • hypochromic anemia   (MGI Ref ID J:15222)
    • microcytic anemia   (MGI Ref ID J:15222)
  • decreased erythrocyte cell number
    • at 7-11 weeks of age, ~90% of homozygotes display decreased erythrocyte numbers relative to wild-type controls   (MGI Ref ID J:15222)
  • decreased hemoglobin content
    • at 7-11 weeks of age, ~90% of homozygotes display a reduced hemoglobin concentration in circulating blood   (MGI Ref ID J:15222)
  • decreased spleen iron level   (MGI Ref ID J:15222)
  • decreased spleen red pulp amount
    • severely anemic homozygotes display hypoplasia of the splenic red pulp   (MGI Ref ID J:15222)
  • increased IgE level
    • total IgE levels are more than 7-fold higher and serum levels of OVA-specific IgE more than 2-fold higher than in wild-type mice after ovalbumin challenge   (MGI Ref ID J:62283)
  • increased IgG1 level
    • OVA-specific IgG1 levels are higher in ovalbumin-sensitized mutants   (MGI Ref ID J:62283)
  • increased IgG2a level
    • OVA-specific IgG2a levels are higher in ovalbumin-sensitized mutants   (MGI Ref ID J:62283)
  • increased thymus weight
    • increases with time and IBD   (MGI Ref ID J:107077)
  • thymus hyperplasia
    • increases with time and IBD   (MGI Ref ID J:107077)
  • immune system phenotype
  • *normal* immune system phenotype   (MGI Ref ID J:107077)
    • B and T lymphocytes develop normally at 4-6 weeks of age, young homozygotes exhibit normal CD4+ and CD8+ T subsets in thymus and spleen as well as normal B cell subsets in bone marrow, spleen and peritoneum relative to wild-type controls   (MGI Ref ID J:15222)
    • young homozygotes show a normal antibody response to alpha (1-3)-dextrane, suggesting a normal B-1 cell subset in the peritoneum   (MGI Ref ID J:15222)
    • young homozygotes display normal antibody production and development of B cell memory in response to T cell-dependent immunization with haptenated chicken gamma-globulin   (MGI Ref ID J:15222)
    • abnormal immune system physiology   (MGI Ref ID J:35020)
      • abnormal Langerhans cell physiology
        • greater numbers of cells migrate to lymph nodes after hapten exposure   (MGI Ref ID J:51636)
      • abnormal cytokine level   (MGI Ref ID J:35020)
        • abnormal interferon level
          • IFNgamma is expressed in colon in mice with minor IBD symptoms   (MGI Ref ID J:107077)
          • increased interferon gamma in the colon   (MGI Ref ID J:35020)
          • elevated amounts of IFN gamma produced by irradiated CD4+ cells   (MGI Ref ID J:125760)
        • abnormal interleukin level
          • Il-2, but not Il-1beta is expressed in colon in mice with minor IBD symptoms   (MGI Ref ID J:107077)
          • production of IL1 alpha is 3-4 times higher than controls 24 hours after LPS stimulation   (MGI Ref ID J:51636)
          • increased IL 1 alpha, IL6, in the colon   (MGI Ref ID J:35020)
          • reduced IL4 production by irradiated CD4+ cells   (MGI Ref ID J:35020)
        • abnormal tumor necrosis factor level
          • TNFalpha is expressed in colon in mice with minor IBD symptoms   (MGI Ref ID J:107077)
          • production of TNF alpha is 3-4 times higher than controls 24 hours after LPS stimulation   (MGI Ref ID J:51636)
          • increased TNF alpha in the colon   (MGI Ref ID J:35020)
      • abnormal level of surface class II molecules   (MGI Ref ID J:15222)
      • abnormal response to infection
        • upon infection with the nematode N. brasiliensis, homozygotes develop a Th1 response in addition to the expected nematode-induced Th2 response, as shown by a 5-fold increase in IFN-gamma levels in culture supernatants of Con A-stimulated spleen cells   (MGI Ref ID J:15222)
        • increased susceptibility to parasitic infection
          • time to death induced by exposure to Plasmodium falciparum is decreased compared to in wild-type mice (7+/-0 days compared to 7.8+/-0.2 days, respectively)   (MGI Ref ID J:123927)
          • in mice depleted of regulatory T cells, experimental cerebral malaria is delayed following exposure to Plasmodium falciparum but disease progression occurs unlike in wild-type mice similarly treated   (MGI Ref ID J:123927)
      • abnormal type IV hypersensitivity reaction
        • blockage of delayed-type hypertension by midrange UV radiation is prevented   (MGI Ref ID J:35510)
        • increased susceptibility to type IV hypersensitivity reaction
          • enhanced contact hypersensitivity to FITC   (MGI Ref ID J:51636)
      • chronic inflammation
        • enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon   (MGI Ref ID J:15222)
        • inflammation was limited to the proximal colon under specific pathogen free conditions   (MGI Ref ID J:15222)
      • decreased T cell proliferation
        • reduced proliferative response of CD4+ cells to UVB irradiation   (MGI Ref ID J:125760)
      • decreased length of allograft survival
        • significantly lower cardiac graft survival times   (MGI Ref ID J:44346)
      • increased IgE level
        • total IgE levels are more than 7-fold higher and serum levels of OVA-specific IgE more than 2-fold higher than in wild-type mice after ovalbumin challenge   (MGI Ref ID J:62283)
      • increased IgG1 level
        • OVA-specific IgG1 levels are higher in ovalbumin-sensitized mutants   (MGI Ref ID J:62283)
      • increased IgG2a level
        • OVA-specific IgG2a levels are higher in ovalbumin-sensitized mutants   (MGI Ref ID J:62283)
      • increased interferon-gamma secretion
        • upon infection with the nematode N. brasiliensis, homozygotes develop a Th1 response in addition to the expected nematode-induced Th2 response, as shown by a 5-fold increase in IFN-gamma levels in culture supernatants of Con A-stimulated spleen cells   (MGI Ref ID J:15222)
        • a similar increase in IFN-gamma production is found in cultures of anti-CD3-stimulated spleenic CD4+ T cells from nematode-infected homozygotes relative to infected controls   (MGI Ref ID J:15222)
      • intestinal inflammation   (MGI Ref ID J:35020)
        • anemic and underweight homozygotes display enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon   (MGI Ref ID J:15222)
        • inflammation was limited to the proximal colon under specific pathogen free conditions   (MGI Ref ID J:15222)
        • spontaneous inflammatory bowel disease (IBD) develops by 5 weeks in some animals   (MGI Ref ID J:107077)
        • large intestinal inflammation
          • lymphocytes and small numbers of neutrophiles as infiltrates in the lamina propria of the cecum, ascending and transverse colon at three weeks   (MGI Ref ID J:35020)
          • multifocal lesions in all regions of the large intestine at three months   (MGI Ref ID J:35020)
          • occasional transmural inflammation and crypt abscesses at 3 months   (MGI Ref ID J:35020)
          • more ulcerations at 6 months   (MGI Ref ID J:35020)
          • cecum inflammation   (MGI Ref ID J:35020)
          • colitis
            • all Il10-null mice develop colitis by the age of 9 weeks in contrast to wild-type littermates   (MGI Ref ID J:68476)
        • small intestinal inflammation
          • 8% with duodenitis at 3 months of age   (MGI Ref ID J:35020)
          • increased duodenitis at 6 months   (MGI Ref ID J:35020)
    • abnormal leukocyte morphology   (MGI Ref ID J:35020)
      • abnormal lymphocyte cell number
        • double control levels in the lamina propria   (MGI Ref ID J:35020)
        • increased CD4-positive T cell number
          • elevated   (MGI Ref ID J:35020)
          • activated memory phenotype   (MGI Ref ID J:35020)
      • decreased T cell proliferation
        • reduced proliferative response of CD4+ cells to UVB irradiation   (MGI Ref ID J:125760)
      • increased granulocyte number
        • homozygotes display up to a 2-fold elevation in leukocyte numbers due to an increase in granulocytes   (MGI Ref ID J:15222)
        • elevated at 3 weeks and increasing with age   (MGI Ref ID J:35020)
    • abnormal myelopoiesis
      • severely anemic homozygotes display a hyperproliferative myeloid compartment   (MGI Ref ID J:15222)
    • decreased spleen iron level   (MGI Ref ID J:15222)
    • decreased spleen red pulp amount
      • severely anemic homozygotes display hypoplasia of the splenic red pulp   (MGI Ref ID J:15222)
    • increased thymus weight
      • increases with time and IBD   (MGI Ref ID J:107077)
    • thymus hyperplasia
      • increases with time and IBD   (MGI Ref ID J:107077)
  • tumorigenesis
  • decreased tumor incidence
    • CD8+ cells impart faster tumor rejection in hosts   (MGI Ref ID J:125760)
    • decreased incidence of tumors by UV induction
      • do not develop skin tumors in response to UVB (280-350nm) exposure, even after 1 year   (MGI Ref ID J:125760)
  • increased intestinal adenocarcinoma incidence
    • at 9 weeks, 13% of homozygotes have adenocarcinomas   (MGI Ref ID J:68476)
    • in 10-31 week old animals, there is a 65% incidence of colorectal carcinomas   (MGI Ref ID J:68476)
    • increased large intestine adenocarcinoma incidence
      • 25% with colorectal adenocarcinomas at 3 months   (MGI Ref ID J:35020)
      • higher incidence of colorectal cancer at 6 months but no metastasis to lymph nodes   (MGI Ref ID J:35020)
  • respiratory system phenotype
  • decreased airway responsiveness
    • mutants sensitized and challenged to ovalbumin (OVA) fail to develop airway hyper-responsiveness despite a significant eosinophilic airway inflammatory response   (MGI Ref ID J:62283)
    • mutants are hyporesponsive to electrical field stimulation of trachea smooth muscle after OVA aerosol challenge   (MGI Ref ID J:62283)
    • airway response to methacholine is reduced by 37%   (MGI Ref ID J:115459)
    • tracheal rings are less responsive to KCl   (MGI Ref ID J:115459)
    • less tension develops (restored by treatment with L-NAME)   (MGI Ref ID J:115459)
  • homeostasis/metabolism phenotype
  • abnormal homeostasis   (MGI Ref ID J:129479)
    • abnormal glucose homeostasis   (MGI Ref ID J:129479)
      • decreased circulating insulin level
        • plasma insulin levels are 55% lower than controls after an overnight fast following 6 weeks on a high fat diet   (MGI Ref ID J:129479)
      • increased insulin sensitivity
        • greater increase in insulin stimulated whole body glucose uptake when corrected for lower plasma insulin   (MGI Ref ID J:129479)
    • abnormal iron level
      • homozygotes display depleted iron stores in spleen and bone marrow   (MGI Ref ID J:15222)
      • decreased circulating iron level
        • homozygotes display a 50% reduction in serum iron levels relative to wild-type controls   (MGI Ref ID J:15222)
      • decreased spleen iron level   (MGI Ref ID J:15222)
    • abnormal lipid level   (MGI Ref ID J:129479)
      • decreased circulating cholesterol level
        • decreased cholesterol esters   (MGI Ref ID J:129479)
      • increased circulating cholesterol level
        • increased free cholesterol   (MGI Ref ID J:129479)
      • increased fatty acid level
        • basal free fatty acid levels are significantly increased   (MGI Ref ID J:129479)
      • increased leukotriene level
        • OVA-sensitized mutants exhibit higher eosinophil peroxidase and leukotriene levels in bronchoalveolar lavage fluid than wild-type mice   (MGI Ref ID J:62283)
      • increased liver triglyceride level
        • 54% increase in hepatic triglycerides relative to controls   (MGI Ref ID J:129479)
        • plasma triglycerides not elevated   (MGI Ref ID J:129479)
    • abnormal nitric oxide homeostasis
      • exhaled NO is significantly decreased   (MGI Ref ID J:115459)
    • abnormal protein level
      • increased phosphorylated protein kinase after insulin stimulation   (MGI Ref ID J:129479)
      • abnormal circulating protein level   (MGI Ref ID J:110238)
        • abnormal circulating enzyme level
          • higher levels of alanine:2-oxaloglutarate aminotransferase in plasma 8 hours after lipopolysaccharide treatment   (MGI Ref ID J:110238)
        • abnormal circulating serum albumin level
      • abnormal cytokine level   (MGI Ref ID J:35020)
        • abnormal interferon level
          • IFNgamma is expressed in colon in mice with minor IBD symptoms   (MGI Ref ID J:107077)
          • increased interferon gamma in the colon   (MGI Ref ID J:35020)
          • elevated amounts of IFN gamma produced by irradiated CD4+ cells   (MGI Ref ID J:125760)
        • abnormal interleukin level
          • Il-2, but not Il-1beta is expressed in colon in mice with minor IBD symptoms   (MGI Ref ID J:107077)
          • production of IL1 alpha is 3-4 times higher than controls 24 hours after LPS stimulation   (MGI Ref ID J:51636)
          • increased IL 1 alpha, IL6, in the colon   (MGI Ref ID J:35020)
          • reduced IL4 production by irradiated CD4+ cells   (MGI Ref ID J:35020)
        • abnormal tumor necrosis factor level
          • TNFalpha is expressed in colon in mice with minor IBD symptoms   (MGI Ref ID J:107077)
          • production of TNF alpha is 3-4 times higher than controls 24 hours after LPS stimulation   (MGI Ref ID J:51636)
          • increased TNF alpha in the colon   (MGI Ref ID J:35020)
    • decreased circulating creatinine level   (MGI Ref ID J:93577)
  • decreased physiological sensitivity to xenobiotic
    • airway response to methacholine is reduced by 37%   (MGI Ref ID J:115459)
  • enhanced wound healing
    • experimental wound is a 6 mm circular excision through the full thickness of the skin   (MGI Ref ID J:117053)
    • macroscopic wound closure is accelerated   (MGI Ref ID J:117053)
    • by day 3, density of vascular structures significantly increased   (MGI Ref ID J:117053)
    • earlier and more persistent influx of greater numbers of macrophage into wound   (MGI Ref ID J:117053)
    • fully epithelialized and scab lost by 7 days   (MGI Ref ID J:117053)
    • increased collagen content and advanced maturation and organization of collagen bundles at 14 days   (MGI Ref ID J:117053)
  • increased myocardial infarction size
    • 90% more necrosis after experimental ischemia and reperfusion than found in controls   (MGI Ref ID J:70292)
    • 60% more polymorphonuclear neutrophiles per unit area in mid-ventricular slices relative to controls   (MGI Ref ID J:70292)
  • endocrine/exocrine gland phenotype
  • abnormal crypts of Lieberkuhn morphology   (MGI Ref ID J:15222)
  • increased thymus weight
    • increases with time and IBD   (MGI Ref ID J:107077)
  • thymus hyperplasia
    • increases with time and IBD   (MGI Ref ID J:107077)
  • behavior/neurological phenotype
  • increased thermal nociceptive threshold
    • latency to paw-licking is significantly longer on a hot plate test   (MGI Ref ID J:119039)
  • cardiovascular system phenotype
  • abnormal placental labyrinth vasculature morphology
    • 26% increase in maternal blood space in the labyrinth   (MGI Ref ID J:113180)
    • fetal capillaries are normal   (MGI Ref ID J:113180)
  • increased myocardial infarction size
    • 90% more necrosis after experimental ischemia and reperfusion than found in controls   (MGI Ref ID J:70292)
    • 60% more polymorphonuclear neutrophiles per unit area in mid-ventricular slices relative to controls   (MGI Ref ID J:70292)
  • craniofacial phenotype
  • abnormal alveolar process morphology
    • 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks   (MGI Ref ID J:147935)
  • embryogenesis phenotype
  • abnormal placental labyrinth vasculature morphology
    • 26% increase in maternal blood space in the labyrinth   (MGI Ref ID J:113180)
    • fetal capillaries are normal   (MGI Ref ID J:113180)
  • increased placental labyrinth size
    • 37% increase in cross-sectional area   (MGI Ref ID J:113180)
  • limbs/digits/tail phenotype
  • short femur   (MGI Ref ID J:93577)
  • liver/biliary system phenotype
  • abnormal liver physiology
    • hepatic glucose production is reduced more than in controls   (MGI Ref ID J:129479)
    • increased hepatocyte apoptosis
      • increased response in liver 4 hours after lipopolysaccharide treatment   (MGI Ref ID J:110238)
  • increased liver triglyceride level
    • 54% increase in hepatic triglycerides relative to controls   (MGI Ref ID J:129479)
    • plasma triglycerides not elevated   (MGI Ref ID J:129479)
  • skeleton phenotype
  • abnormal skeleton morphology   (MGI Ref ID J:93577)
    • abnormal alveolar process morphology
      • 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks   (MGI Ref ID J:147935)
    • abnormal bone structure   (MGI Ref ID J:93577)
      • abnormal osteoblast differentiation
        • decreased osteoblast generation in primary bone marrow stromal culture   (MGI Ref ID J:93577)
        • 40% fewer mineralized bone-like nodules in bone marrow cell culture   (MGI Ref ID J:93577)
      • abnormal trabecular bone morphology
        • reduced trabecular bone surface   (MGI Ref ID J:93577)
        • decreased bone trabecula number
          • reduced trabecular number   (MGI Ref ID J:93577)
        • decreased trabecular bone mass
          • cancellous bone mass of the tibia significantly decreased   (MGI Ref ID J:93577)
          • trabecular bone further reduced in mice with colitis   (MGI Ref ID J:93577)
        • decreased trabecular bone thickness
          • reduced trabecular width   (MGI Ref ID J:93577)
      • decreased bone mineral content
        • significantly reduced femoral ash weight   (MGI Ref ID J:93577)
      • decreased compact bone mass
        • cortical bone mass reduced   (MGI Ref ID J:93577)
    • short femur   (MGI Ref ID J:93577)
  • abnormal skeleton physiology   (MGI Ref ID J:93577)
    • abnormal bone mineralization
      • cancellous mineral apposition rate and bone formation rate are reduced   (MGI Ref ID J:93577)
      • bone resorption is normal   (MGI Ref ID J:93577)
    • decreased bone strength
      • femora more fragile in mechanical load tests   (MGI Ref ID J:93577)
      • reduced stiffness of femora   (MGI Ref ID J:93577)
  • integument phenotype
  • increased thermal nociceptive threshold
    • latency to paw-licking is significantly longer on a hot plate test   (MGI Ref ID J:119039)
  • cellular phenotype
  • abnormal osteoblast differentiation
    • decreased osteoblast generation in primary bone marrow stromal culture   (MGI Ref ID J:93577)
    • 40% fewer mineralized bone-like nodules in bone marrow cell culture   (MGI Ref ID J:93577)
  • increased hepatocyte apoptosis
    • increased response in liver 4 hours after lipopolysaccharide treatment   (MGI Ref ID J:110238)

Il10tm1Cgn/Il10tm1Cgn

        involves: 129P2/OlaHsd
  • reproductive system phenotype
  • abnormal reproductive system physiology
    • mice treated with Gal1 exhibit less protection from stress-induced fetal loss compared to similarly treated wild-type mice   (MGI Ref ID J:130208)
  • immune system phenotype
  • abnormal cytokine secretion
    • 6 hours after LPS injection, TNF, Il12 and Ifng levels are substantially higher than in controls   (MGI Ref ID J:117122)
  • abnormal inflammatory response
    • after three subcutaneous injections of LPS into the flank, mice develop solid subcutaneous swellings whereas wild-type do not   (MGI Ref ID J:117122)
    • lesion is associated with infiltration of macrophages and neutrophils, edema, and extensive necrosis of dermal, epidermal, and muscle layers of skin   (MGI Ref ID J:117122)
    • 5 days after flank injection of CpG, mice develop solid subcutaneous swellings at the injection site; lesions show conspicuous edema, massive infiltration by macrophages and neutrophilic granulocytes, and extensive necrosis of the dermis, epidermis and muscle layer of the skin while lesions in controls do not display edema or necrosis and show infiltration by macrophages primarily   (MGI Ref ID J:117122)
    • increased susceptibility to endotoxin shock
      • i.p. injection of LPS results in death in all animal by 48 hours, compared to survival of 23/25 controls   (MGI Ref ID J:117122)
      • LPS-treated mice exhibit uncontrollable release of IL12 and TNF-alpha compared with wild-type mice   (MGI Ref ID J:118833)
    • intestinal inflammation
      • mice show exaggerated inflammatory response upon exposure to CML-mps-containing eluate compared to control   (MGI Ref ID J:113376)
  • increased circulating interleukin-12 level
    • in LPS-treated mice   (MGI Ref ID J:118833)
  • increased circulating tumor necrosis factor level
    • in LPS-treated mice   (MGI Ref ID J:118833)
  • digestive/alimentary phenotype
  • intestinal inflammation
    • mice show exaggerated inflammatory response upon exposure to CML-mps-containing eluate compared to control   (MGI Ref ID J:113376)
  • homeostasis/metabolism phenotype
  • increased circulating interleukin-12 level
    • in LPS-treated mice   (MGI Ref ID J:118833)
  • increased circulating tumor necrosis factor level
    • in LPS-treated mice   (MGI Ref ID J:118833)

Il10tm1Cgn/Il10tm1Cgn

        B6.129P2-Il10tm1Cgn/J
  • growth/size/body phenotype
  • slow postnatal weight gain
    • lower body weight gain between 5 and 10 weeks of age than for controls   (MGI Ref ID J:124308)
  • immune system phenotype
  • abnormal cytokine level
    • in LPS-injected mice   (MGI Ref ID J:157787)
    • levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment   (MGI Ref ID J:139972)
    • abnormal chemokine level
      • LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice   (MGI Ref ID J:157787)
    • increased circulating interferon-gamma level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-1 alpha level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-1 beta level
      • in LPS-injected mice   (MGI Ref ID J:157787)
      • plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls   (MGI Ref ID J:139972)
    • increased circulating interleukin-12 level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-17 level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-2 level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-6 level
      • slightly in LPS-injected mice   (MGI Ref ID J:157787)
      • plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls   (MGI Ref ID J:139972)
    • increased circulating tumor necrosis factor level
      • in LPS-injected mice   (MGI Ref ID J:157787)
  • abnormal regulatory T cell physiology
    • CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nażve CD4 T cells into immunodeficient hosts   (MGI Ref ID J:125748)
    • however, CD25-postive CD4 T cells inhibit the expansion of naive T cells in Rag2 deficient hosts as effectively as wild-type CD25-positive CD4 T cells   (MGI Ref ID J:125748)
  • increased susceptibility to parasitic infection
    • mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice   (MGI Ref ID J:157787)
  • large intestinal inflammation
    • mutants develop severe inflammation in the colon leading to inflammatory bowel disease   (MGI Ref ID J:149347)
    • cecum inflammation
      • mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice   (MGI Ref ID J:157787)
    • increased susceptibility to induced colitis
      • upon DSS exposure   (MGI Ref ID J:157787)
  • homeostasis/metabolism phenotype
  • abnormal cytokine level
    • in LPS-injected mice   (MGI Ref ID J:157787)
    • levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment   (MGI Ref ID J:139972)
    • abnormal chemokine level
      • LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice   (MGI Ref ID J:157787)
    • increased circulating interferon-gamma level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-1 alpha level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-1 beta level
      • in LPS-injected mice   (MGI Ref ID J:157787)
      • plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls   (MGI Ref ID J:139972)
    • increased circulating interleukin-12 level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-17 level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-2 level
      • in LPS-injected mice   (MGI Ref ID J:157787)
    • increased circulating interleukin-6 level
      • slightly in LPS-injected mice   (MGI Ref ID J:157787)
      • plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls   (MGI Ref ID J:139972)
    • increased circulating tumor necrosis factor level
      • in LPS-injected mice   (MGI Ref ID J:157787)
  • impaired adaptive thermogenesis
    • lipopolysaccharide causes a very significant drop in core body temperature   (MGI Ref ID J:114404)
  • impaired exercise endurance
    • time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment   (MGI Ref ID J:139972)
  • increased cerebral infarction size
    • lesion volume after middle cerebral artery occlusion increases 30%   (MGI Ref ID J:108086)
  • increased susceptibility to neuronal excitotoxicity
    • increased toxicity of N-methyl-D-aspartate in primary neuron culture   (MGI Ref ID J:108086)
  • digestive/alimentary phenotype
  • large intestinal inflammation
    • mutants develop severe inflammation in the colon leading to inflammatory bowel disease   (MGI Ref ID J:149347)
    • cecum inflammation
      • mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice   (MGI Ref ID J:157787)
    • increased susceptibility to induced colitis
      • upon DSS exposure   (MGI Ref ID J:157787)
  • rectal prolapse
    • rectal prolapse is seen at a median time of 16 weeks of age   (MGI Ref ID J:149347)
  • cardiovascular system phenotype
  • decreased mean systemic arterial blood pressure
    • lower under basal conditions   (MGI Ref ID J:146372)
  • decreased susceptibility to induced choroidal neovascularization
    • reduced choroidal neovascularization 7 days following krypton laser exposure of the eye   (MGI Ref ID J:134144)
  • decreased vasoconstriction
    • LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine   (MGI Ref ID J:59742)
  • increased vasoconstriction
    • endothelin 1 induced contraction of Aorta and first order mesenteric arteries is greater than controls when also treated with L-NAME and indomethecine and TNFalpha   (MGI Ref ID J:146372)
    • response to endothelin 1 is eliminated in the presence of PD-98059   (MGI Ref ID J:146372)
  • muscle phenotype
  • decreased vasoconstriction
    • LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine   (MGI Ref ID J:59742)
  • increased vasoconstriction
    • endothelin 1 induced contraction of Aorta and first order mesenteric arteries is greater than controls when also treated with L-NAME and indomethecine and TNFalpha   (MGI Ref ID J:146372)
    • response to endothelin 1 is eliminated in the presence of PD-98059   (MGI Ref ID J:146372)
  • behavior/neurological phenotype
  • abnormal sleep pattern
    • more time in "slow-wave sleep" and less time awake during dark phase   (MGI Ref ID J:114404)
    • less effect of influenza virus infection on slow wave sleep during dark phase but a greater decrease in delta wave amplitude   (MGI Ref ID J:114404)
    • lipopolysaccharide causes an overall decrease in delta wave amplitude   (MGI Ref ID J:114404)
    • lipopolysaccharide causes decreased slow wave and REM sleep during light phase   (MGI Ref ID J:114404)
    • lipopolysaccharide results in increased time spent awake, particularly in light phase   (MGI Ref ID J:114404)
  • impaired coordination
    • rotarod performance worsens after IP lipopolysaccharide injection   (MGI Ref ID J:139972)
    • effect persists at least 24 hours   (MGI Ref ID J:139972)
    • performance fails to improve over consecutive trials but only after IP lipopolysaccharide injection   (MGI Ref ID J:139972)
  • impaired exercise endurance
    • time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment   (MGI Ref ID J:139972)
  • nervous system phenotype
  • abnormal neuron physiology
    • increased sensitivity to oxygen or glucose deprivation   (MGI Ref ID J:108086)
    • increased susceptibility to neuronal excitotoxicity
      • increased toxicity of N-methyl-D-aspartate in primary neuron culture   (MGI Ref ID J:108086)
  • increased cerebral infarction size
    • lesion volume after middle cerebral artery occlusion increases 30%   (MGI Ref ID J:108086)
  • vision/eye phenotype
  • decreased susceptibility to induced choroidal neovascularization
    • reduced choroidal neovascularization 7 days following krypton laser exposure of the eye   (MGI Ref ID J:134144)
  • tumorigenesis
  • increased colon adenocarcinoma incidence
    • 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas   (MGI Ref ID J:149347)
    • tumors develop between 25 and 35 weeks of age   (MGI Ref ID J:149347)
  • cellular phenotype
  • increased susceptibility to neuronal excitotoxicity
    • increased toxicity of N-methyl-D-aspartate in primary neuron culture   (MGI Ref ID J:108086)
  • hematopoietic system phenotype
  • abnormal regulatory T cell physiology
    • CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring nażve CD4 T cells into immunodeficient hosts   (MGI Ref ID J:125748)
    • however, CD25-postive CD4 T cells inhibit the expansion of naive T cells in Rag2 deficient hosts as effectively as wild-type CD25-positive CD4 T cells   (MGI Ref ID J:125748)

Il10tm1Cgn/Il10tm1Cgn

        involves: 129P2/OlaHsd * C57BL/6 * DBA/1
  • growth/size/body phenotype
  • decreased body weight
    • lower body weight than controls   (MGI Ref ID J:84100)
  • digestive/alimentary phenotype
  • colitis
    • increased lymphocytes in the lamina propria   (MGI Ref ID J:84100)
    • inflamatory cells in the mucosa   (MGI Ref ID J:84100)
    • epithelial hyperplasia   (MGI Ref ID J:84100)
    • reduced mucin producing goblet cells   (MGI Ref ID J:84100)
  • immune system phenotype
  • colitis
    • increased lymphocytes in the lamina propria   (MGI Ref ID J:84100)
    • inflamatory cells in the mucosa   (MGI Ref ID J:84100)
    • epithelial hyperplasia   (MGI Ref ID J:84100)
    • reduced mucin producing goblet cells   (MGI Ref ID J:84100)

Il10tm1Cgn/Il10tm1Cgn

        involves: 129P2/OlaHsd * 129S/SvEv
  • growth/size/body phenotype
  • decreased body weight
    • mice older than 4 weeks weigh significantly less than controls   (MGI Ref ID J:59872)
  • digestive/alimentary phenotype
  • abnormal intestine physiology
    • increased colon permeability to mannitol at 2, 4, and 10weeks but not under germ free conditions   (MGI Ref ID J:59872)
    • ileal permeability to mannitol 3X higher than in controls at 2 weeks but normal at 6 weeks   (MGI Ref ID J:59872)
    • more IFNgamma and TNFalpha produced in the ileum and colon than in controls   (MGI Ref ID J:59872)
    • colonic iNOS production increases with age after 4 weeks   (MGI Ref ID J:59872)
    • colitis
      • mild colitis at 4 weeks which plateaus by 8 weeks   (MGI Ref ID J:59872)
      • no ileal injury through 16 weeks   (MGI Ref ID J:59872)
      • no colitis when raised in germ free conditions   (MGI Ref ID J:59872)
  • immune system phenotype
  • colitis
    • mild colitis at 4 weeks which plateaus by 8 weeks   (MGI Ref ID J:59872)
    • no ileal injury through 16 weeks   (MGI Ref ID J:59872)
    • no colitis when raised in germ free conditions   (MGI Ref ID J:59872)

Il10tm1Cgn/Il10tm1Cgn

        129S.Cg-Il10tm1Cgn
  • cardiovascular system phenotype
  • decreased vasoconstriction
    • LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine   (MGI Ref ID J:59742)
  • muscle phenotype
  • decreased vasoconstriction
    • LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine   (MGI Ref ID J:59742)

Il10tm1Cgn/Il10tm1Cgn

        B10.129P2(B6)-Il10tm1Cgn/J
  • immune system phenotype
  • decreased length of allograft survival
    • decrease in survival times of heart transplants from BALB/c mice after a 30 day course of anti-CD4 and anti-CD8 mAb   (MGI Ref ID J:44346)
    • acute rejection severity of cardiac allografts (BALB/c) is increased compared to wild-type controls   (MGI Ref ID J:44346)

Il10tm1Cgn/Il10tm1Cgn

        B6.129P2-Il10tm1Cgn
  • immune system phenotype
  • abnormal circulating interleukin-12b level
    • PGE2 represses LPS induction to a lesser extent than it does in controls   (MGI Ref ID J:191723)
  • abnormal circulating interleukin-6 level
    • PGE2 represses LPS induction to a lesser extent than it does in controls   (MGI Ref ID J:191723)
  • homeostasis/metabolism phenotype
  • abnormal circulating interleukin-12b level
    • PGE2 represses LPS induction to a lesser extent than it does in controls   (MGI Ref ID J:191723)
  • abnormal circulating interleukin-6 level
    • PGE2 represses LPS induction to a lesser extent than it does in controls   (MGI Ref ID J:191723)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Il10tm1Cgn related

Cancer Research
Growth Factors/Receptors/Cytokines

Hematological Research
Anemia, Iron Deficiency and Transport Defects
      hemolytic
Immunological Defects

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
Growth Factors/Receptors/Cytokines
Immunodeficiency
Inflammation
      Inflammatory bowel disease

Pde6brd1 related

Sensorineural Research
Retinal Degeneration

Tlr4Lps-d related

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
      Tlr deficiency
Immunodeficiency
      Tlr deficiency
Inflammation
      Tlr deficiency

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Il10tm1Cgn
Allele Name targeted mutation 1, University of Cologne
Allele Type Targeted (Null/Knockout)
Common Name(s) IL-10 KO; IL-10-; IL-10KO; IL-10KO; Il10-; Il10tmCgn;
Mutation Made ByDr. Ralf Kuhn,   University of Cologne
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14.1
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Il10, interleukin 10
Chromosome 1
Gene Common Name(s) CSIF; GVHDS; IL-10; IL10A; IL10X; Il-10; TGIF; cytokine synthesis inhibitory factor;
General Note Phenotypic Similarity to Human Syndrome: Idiopathic Inflammatory Bowel Disease (J:15222).
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. [MGI Ref ID J:15222]
 
Allele Symbol Pde6brd1
Allele Name retinal degeneration 1
Allele Type Spontaneous
Common Name(s) Pdebrd1; rd; rd-1; rd1; rodless retina;
Strain of Originvarious
Gene Symbol and Name Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Chromosome 5
Gene Common Name(s) CSNB3; CSNBAD2; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10;
General Note The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
Molecular Note Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361]
 
Allele Symbol Tlr4Lps-d
Allele Name defective lipopolysaccharide response
Allele Type Spontaneous
Common Name(s) TLR4-M; TLR4-Mu; TLR4lps-def; TLR4d; Tlr4-; Tlr4d; TlrLps-d; lpsd; mutant TLR4;
Strain of OriginC3H/HeJ
Gene Symbol and Name Tlr4, toll-like receptor 4
Chromosome 4
Gene Common Name(s) ARMD10; CD284; Lps; RAS-like, family 2, locus 8; Rasl2-8; TLR-4; TOLL; lipopolysaccharide response;
General Note C3H/HeJ mice carry this allele. Various combinations of Lps-associated traits have been followed in crosses between C3H/HeJ and other C3H substrains, and the traits have in all cases segregated together (J:30692, J:5557, J:5593, J:5938). Some of the traits show dominance of the Tlr4lps-n allele; others, including Tlr4Lps-d, show codominance.

Genbank ID for this allele: AF095353

Molecular Note This allele corresponds to a mutation in the third exon of the gene. A C to A substitution at nucleotide position 2342 results in an amino acid substitution that replaces proline with histidine at position 712. [MGI Ref ID J:51522] [MGI Ref ID J:53519] [MGI Ref ID J:57938]

Genotyping

Genotyping Information

Genotyping Protocols

Il10tm1Cgn, Melt Curve Analysis
Il10tm1Cgn, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Bristol IJ; Farmer MA; Cong Y; Zheng XX; Strom TB; Elson CO; Sundberg JP; Leiter EH. 2000. Heritable susceptibility for colitis in mice induced by IL-10 deficiency. Inflamm Bowel Dis 6(4):290-302. [PubMed: 11149562]  [MGI Ref ID J:109882]

Additional References

Kuhn R; Lohler J; Rennick D; Rajewsky K; Muller W. 1993. Interleukin-10-deficient mice develop chronic enterocolitis [see comments] Cell 75(2):263-74. [PubMed: 8402911]  [MGI Ref ID J:15222]

Il10tm1Cgn related

Aggarwal NR; Tsushima K; Eto Y; Tripathi A; Mandke P; Mock JR; Garibaldi BT; Singer BD; Sidhaye VK; Horton MR; King LS; D'Alessio FR. 2014. Immunological priming requires regulatory T cells and IL-10-producing macrophages to accelerate resolution from severe lung inflammation. J Immunol 192(9):4453-64. [PubMed: 24688024]  [MGI Ref ID J:209966]

Akhiani AA; Stensson A; Schon K; Lycke NY. 2005. IgA antibodies impair resistance against Helicobacter pylori infection: studies on immune evasion in IL-10-deficient mice. J Immunol 174(12):8144-53. [PubMed: 15944323]  [MGI Ref ID J:100891]

Alayan J; Ivanovski S; Farah CS. 2007. Alveolar bone loss in T helper 1/T helper 2 cytokine-deficient mice. J Periodontal Res 42(2):97-103. [PubMed: 17305866]  [MGI Ref ID J:147935]

Albert E; Walker J; Thiesen A; Churchill T; Madsen K. 2010. cis-Urocanic acid attenuates acute dextran sodium sulphate-induced intestinal inflammation. PLoS One 5(10):e13676. [PubMed: 21060867]  [MGI Ref ID J:166665]

Aliberti J; Viola JP; Vieira-de-Abreu A; Bozza PT; Sher A; Scharfstein J. 2003. Cutting edge: Bradykinin induces IL-12 production by dendritic cells: a danger signal that drives Th1 polarization. J Immunol 170(11):5349-53. [PubMed: 12759407]  [MGI Ref ID J:83453]

Allen HL; Deepe GS Jr. 2005. Apoptosis modulates protective immunity to the pathogenic fungus Histoplasma capsulatum. J Clin Invest 115(10):2875-85. [PubMed: 16151533]  [MGI Ref ID J:101533]

Allen HL; Deepe GS Jr. 2006. B cells and CD4-CD8- T cells are key regulators of the severity of reactivation histoplasmosis. J Immunol 177(3):1763-71. [PubMed: 16849486]  [MGI Ref ID J:138028]

Almeida AR; Legrand N; Papiernik M; Freitas AA. 2002. Homeostasis of peripheral CD4+ T cells: IL-2R alpha and IL-2 shape a population of regulatory cells that controls CD4+ T cell numbers. J Immunol 169(9):4850-60. [PubMed: 12391195]  [MGI Ref ID J:125748]

Amante FH; Stanley AC; Randall LM; Zhou Y; Haque A; McSweeney K; Waters AP; Janse CJ; Good MF; Hill GR; Engwerda CR. 2007. A role for natural regulatory T cells in the pathogenesis of experimental cerebral malaria. Am J Pathol 171(2):548-59. [PubMed: 17600128]  [MGI Ref ID J:123927]

Ameredes BT; Sethi JM; Liu HL; Choi AM; Calhoun WJ. 2005. Enhanced nitric oxide production associated with airway hyporesponsiveness in the absence of IL-10. Am J Physiol Lung Cell Mol Physiol 288(5):L868-73. [PubMed: 15618456]  [MGI Ref ID J:115459]

Ameredes BT; Zamora R; Gibson KF; Billiar TR; Dixon-McCarthy B; Watkins S; Calhoun WJ. 2001. Increased nitric oxide production by airway cells of sensitized and challenged IL-10 knockout mice. J Leukoc Biol 70(5):730-6. [PubMed: 11698492]  [MGI Ref ID J:124461]

Ameredes BT; Zamora R; Sethi JM; Liu HL; Kohut LK; Gligonic AL; Choi AM; Calhoun WJ. 2005. Alterations in nitric oxide and cytokine production with airway inflammation in the absence of IL-10. J Immunol 175(2):1206-13. [PubMed: 16002724]  [MGI Ref ID J:100726]

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Zampell JC; Elhadad S; Avraham T; Weitman E; Aschen S; Yan A; Mehrara BJ. 2012. Toll-like receptor deficiency worsens inflammation and lymphedema after lymphatic injury. Am J Physiol Cell Physiol 302(4):C709-19. [PubMed: 22049214]  [MGI Ref ID J:180614]

Zanotti G; Casiraghi M; Abano JB; Tatreau JR; Sevala M; Berlin H; Smyth S; Funkhouser WK; Burridge K; Randell SH; Egan TM. 2009. Novel critical role of Toll-like receptor 4 in lung ischemia-reperfusion injury and edema. Am J Physiol Lung Cell Mol Physiol 297(1):L52-63. [PubMed: 19376887]  [MGI Ref ID J:151006]

Zhang B; Choi JJ; Eum SY; Daunert S; Toborek M. 2013. TLR4 signaling is involved in brain vascular toxicity of PCB153 bound to nanoparticles. PLoS One 8(5):e63159. [PubMed: 23690990]  [MGI Ref ID J:202173]

Zhang X; Shan P; Jiang G; Cohn L; Lee PJ. 2006. Toll-like receptor 4 deficiency causes pulmonary emphysema. J Clin Invest 116(11):3050-9. [PubMed: 17053835]  [MGI Ref ID J:114985]

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Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryWhen 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.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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