Overview

Also Known As: Il-10 KO

B6.129P2-Il10^tm1Cgn/J mutant mice spontaneously develop a chronic inflammatory bowel disease (IBD). Il10-deficiency 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. Il10-deficient mice exhibit a significant increase in peripheral blood granulocyte populations upon lesion development.

Donating Investigator

Herbert C. Morse III, Laboratory of Immunopathology, NIAID, NI

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

Il10^tm1Cgn

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Il10	interleukin 10

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Research Applications

Immunology, Inflammation and Autoimmunity Research
Cancer Research
Hematological Research

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Base Price

Starting at:

$136.05 Domestic price for female 3-week

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Details

Detailed Description

Mice homozygous for the Il10^tm1Cgn 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).

Development

The Il10^tm1Cgn 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 C57BL/6J genetic background for several generations to generate this strain.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

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

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Genetics

Il10^tm1Cgn

Allele Symbol: Il10^tm1Cgn

Allele Name	targeted mutation 1, University of Cologne
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	targeted mutation 1, University of Cologne; Il10^tm1Cgn
Gene Symbol and Name	Il10, interleukin 10
Gene Synonym(s)	CSIF; cytokine synthesis inhibitory factor; TGIF; IL-10; GVHDS; IL10A; IL10X; Il-10
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

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

inflammatory bowel disease

Research Areas By Genotype

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

Genotype: Il10^tm1Cgn related

Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
- Growth Factors/Receptors/Cytokines
- Immunodeficiency
- Inflammation
  - Inflammatory bowel disease
Cancer Research
- Growth Factors/Receptors/Cytokines
Hematological Research
- Immunological Defects
- Anemia, Iron Deficiency and Transport Defects
  - hemolytic

Mammalian Phenotype Terms by Genotype

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

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6

behavior/neurological phenotype

increased thermal nociceptive threshold
- latency to paw-licking is significantly longer on a hot plate test

craniofacial phenotype

alveolar process atrophy
- 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

immune system phenotype

abnormal cytokine level

abnormal immune system physiology

abnormal interferon level
- elevated amounts of IFN gamma produced by irradiated CD4+ cells
- IFNgamma is expressed in colon in mice with minor IBD symptoms
- increased interferon gamma in the colon

abnormal interleukin level
- Il-2, but not Il-1beta is expressed in colon in mice with minor IBD symptoms
- increased IL 1 alpha, IL6, in the colon
- production of IL1 alpha is 3-4 times higher than controls 24 hours after LPS stimulation
- reduced IL4 production by irradiated CD4+ cells

abnormal Langerhans cell physiology
- greater numbers of cells migrate to lymph nodes after hapten exposure

abnormal leukocyte morphology

abnormal level of surface class II molecules

abnormal lymphocyte cell number
- double control levels in the lamina propria

abnormal myelopoiesis
- severely anemic homozygotes display a hyperproliferative myeloid compartment

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

abnormal tumor necrosis factor level
- increased TNF alpha in the colon
- production of TNF alpha is 3-4 times higher than controls 24 hours after LPS stimulation
- TNFalpha is expressed in colon in mice with minor IBD symptoms

abnormal type IV hypersensitivity reaction
- blockage of delayed-type hypertension by midrange UV radiation is prevented

cecum inflammation

chronic inflammation
- enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon
- inflammation was limited to the proximal colon under specific pathogen free conditions

colitis
- all Il10-null mice develop colitis by the age of 9 weeks in contrast to wild-type littermates

decreased length of allograft survival
- significantly lower cardiac graft survival times

decreased spleen iron level

decreased spleen red pulp amount
- severely anemic homozygotes display hypoplasia of the splenic red pulp

decreased T cell proliferation
- reduced proliferative response of CD4+ cells to UVB irradiation

increased CD4-positive, alpha beta T cell number
- activated memory phenotype
- elevated

increased granulocyte number
- elevated at 3 weeks and increasing with age
- homozygotes display up to a 2-fold elevation in leukocyte numbers due to an increase in granulocytes

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

increased IgG1 level
- OVA-specific IgG1 levels are higher in ovalbumin-sensitized mutants

increased IgG2a level
- OVA-specific IgG2a levels are higher in ovalbumin-sensitized mutants

increased interferon-gamma secretion
- 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
- 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

increased susceptibility to parasitic infection
- 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
- 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)

increased susceptibility to type IV hypersensitivity reaction
- enhanced contact hypersensitivity to FITC

increased thymus weight
- increases with time and IBD

intestinal inflammation
- anemic and underweight homozygotes display enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon
- inflammation was limited to the proximal colon under specific pathogen free conditions
- spontaneous inflammatory bowel disease (IBD) develops by 5 weeks in some animals

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
- more ulcerations at 6 months
- multifocal lesions in all regions of the large intestine at three months
- occasional transmural inflammation and crypt abscesses at 3 months

small intestinal inflammation
- 8% with duodenitis at 3 months of age
- increased duodenitis at 6 months

thymus hyperplasia
- increases with time and IBD

digestive/alimentary phenotype

abnormal colon morphology
- colonic prolapse is observed in some older mutants

abnormal crypts of Lieberkuhn morphology

abnormal enterocyte morphology

abnormal intestinal epithelium morphology

abnormal intestinal mucosa morphology
- at 9 weeks, 59% of mice displaying colitis develop a high grade dysplasia of the colonic mucosa

abnormal large intestine morphology
- minimal epithelial hyperplasia at 3 weeks
- prominent epithelial hyperplasia at 3 months

cecum inflammation

colitis
- all Il10-null mice develop colitis by the age of 9 weeks in contrast to wild-type littermates

increased intestinal adenocarcinoma incidence
- at 9 weeks, 13% of homozygotes have adenocarcinomas
- in 10-31 week old animals, there is a 65% incidence of colorectal carcinomas

increased large intestine adenocarcinoma incidence
- 25% with colorectal adenocarcinomas at 3 months
- higher incidence of colorectal cancer at 6 months but no metastasis to lymph nodes

intestinal inflammation
- anemic and underweight homozygotes display enterocolitis involving the entire intestinal tract, duodenum, proximal jejunum, and proximal colon
- inflammation was limited to the proximal colon under specific pathogen free conditions
- spontaneous inflammatory bowel disease (IBD) develops by 5 weeks in some animals

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
- more ulcerations at 6 months
- multifocal lesions in all regions of the large intestine at three months
- occasional transmural inflammation and crypt abscesses at 3 months

small intestinal inflammation
- 8% with duodenitis at 3 months of age
- increased duodenitis at 6 months

integument phenotype

increased thermal nociceptive threshold
- latency to paw-licking is significantly longer on a hot plate test

limbs/digits/tail phenotype

short femur

liver/biliary system phenotype

abnormal liver physiology
- hepatic glucose production is reduced more than in controls

increased hepatocyte apoptosis
- increased response in liver 4 hours after lipopolysaccharide treatment

increased liver triglyceride level
- 54% increase in hepatic triglycerides relative to controls
- plasma triglycerides not elevated

mammalian phenotype

immune system phenotype
- Normal - 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
- B and T lymphocytes develop normally
- Normal - young homozygotes display normal antibody production and development of B cell memory in response to T cell-dependent immunization with haptenated chicken gamma-globulin
- Normal - young homozygotes show a normal antibody response to alpha (1-3)-dextrane, suggesting a normal B-1 cell subset in the peritoneum

mortality/aging

premature death
- ~30% of homozygotes succumb to disease within 3 months of age
- at >3 months of age, mortality is increased but never reaches 100%
- death is correlated with anemia and gradual weight loss

neoplasm

decreased incidence of tumors by UV induction
- do not develop skin tumors in response to UVB (280-350nm) exposure, even after 1 year

decreased tumor incidence
- CD8+ cells impart faster tumor rejection in hosts

increased intestinal adenocarcinoma incidence
- at 9 weeks, 13% of homozygotes have adenocarcinomas
- in 10-31 week old animals, there is a 65% incidence of colorectal carcinomas

increased large intestine adenocarcinoma incidence
- 25% with colorectal adenocarcinomas at 3 months
- higher incidence of colorectal cancer at 6 months but no metastasis to lymph nodes

respiratory system phenotype

decreased airway responsiveness
- airway response to methacholine is reduced by 37%
- less tension develops (restored by treatment with L-NAME)
- mutants are hyporesponsive to electrical field stimulation of trachea smooth muscle after OVA aerosol challenge
- mutants sensitized and challenged to ovalbumin (OVA) fail to develop airway hyper-responsiveness despite a significant eosinophilic airway inflammatory response
- tracheal rings are less responsive to KCl

skeleton phenotype

abnormal bone mineralization
- Normal - bone resorption is normal
- cancellous mineral apposition rate and bone formation rate are reduced

abnormal bone structure

abnormal osteoblast differentiation
- 40% fewer mineralized bone-like nodules in bone marrow cell culture
- decreased osteoblast generation in primary bone marrow stromal culture

abnormal skeleton morphology

abnormal skeleton physiology

abnormal trabecular bone morphology
- reduced trabecular bone surface

alveolar process atrophy
- 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

decreased bone mineral content
- significantly reduced femoral ash weight

decreased bone strength
- femora more fragile in mechanical load tests
- reduced stiffness of femora

decreased bone trabecula number
- reduced trabecular number

decreased compact bone mass
- cortical bone mass reduced

decreased trabecular bone mass
- cancellous bone mass of the tibia significantly decreased
- trabecular bone further reduced in mice with colitis

decreased trabecular bone thickness
- reduced trabecular width

short femur

cardiovascular system phenotype

abnormal placental labyrinth vasculature morphology
- 26% increase in maternal blood space in the labyrinth
- Normal - fetal capillaries are normal

increased myocardial infarction size
- 60% more polymorphonuclear neutrophiles per unit area in mid-ventricular slices relative to controls
- 90% more necrosis after experimental ischemia and reperfusion than found in controls

embryo phenotype

abnormal placental labyrinth vasculature morphology
- 26% increase in maternal blood space in the labyrinth
- Normal - fetal capillaries are normal

increased placental labyrinth size
- 37% increase in cross-sectional area

endocrine/exocrine gland phenotype

abnormal crypts of Lieberkuhn morphology

increased thymus weight
- increases with time and IBD

thymus hyperplasia
- increases with time and IBD

growth/size/body region phenotype

alveolar process atrophy
- 3 fold increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

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
- at 7-11 weeks of age, most homozygotes display a ~30% weight reduction relative to wild-type controls

postnatal growth retardation
- at 7-11 weeks of age, ~75% of homozygotes are growth retarded relative to wild-type controls
- growth retardation is first observed between 3 and 4 weeks of age

hematopoietic system phenotype

abnormal leukocyte morphology

abnormal lymphocyte cell number
- double control levels in the lamina propria

abnormal myelopoiesis
- severely anemic homozygotes display a hyperproliferative myeloid compartment

absent erythroid progenitor cell
- severely anemic homozygotes show complete depletion of eythroid cells in the bone marrow

anemia
- at 7-11 weeks of age, ~90% of homozygotes exhibit anemia, most likely due to iron deficiency
- the observed anemia is most often defined as microcytic or normocytic and hypochromic

decreased erythrocyte cell number
- at 7-11 weeks of age, ~90% of homozygotes display decreased erythrocyte numbers relative to wild-type controls

decreased hemoglobin content
- at 7-11 weeks of age, ~90% of homozygotes display a reduced hemoglobin concentration in circulating blood

decreased spleen iron level

decreased spleen red pulp amount
- severely anemic homozygotes display hypoplasia of the splenic red pulp

decreased T cell proliferation
- reduced proliferative response of CD4+ cells to UVB irradiation

hypochromic anemia

increased CD4-positive, alpha beta T cell number
- activated memory phenotype
- elevated

increased granulocyte number
- elevated at 3 weeks and increasing with age
- homozygotes display up to a 2-fold elevation in leukocyte numbers due to an increase in granulocytes

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

increased IgG1 level
- OVA-specific IgG1 levels are higher in ovalbumin-sensitized mutants

increased IgG2a level
- OVA-specific IgG2a levels are higher in ovalbumin-sensitized mutants

increased thymus weight
- increases with time and IBD

microcytic anemia

thymus hyperplasia
- increases with time and IBD

cellular phenotype

abnormal osteoblast differentiation
- 40% fewer mineralized bone-like nodules in bone marrow cell culture
- decreased osteoblast generation in primary bone marrow stromal culture

decreased T cell proliferation
- reduced proliferative response of CD4+ cells to UVB irradiation

increased hepatocyte apoptosis
- increased response in liver 4 hours after lipopolysaccharide treatment

homeostasis/metabolism phenotype

abnormal circulating enzyme level
- higher levels of alanine:2-oxaloglutarate aminotransferase in plasma 8 hours after lipopolysaccharide treatment

abnormal circulating protein level

abnormal circulating serum albumin level
- reduced

abnormal cytokine level

abnormal glucose homeostasis

abnormal homeostasis

abnormal interferon level
- elevated amounts of IFN gamma produced by irradiated CD4+ cells
- IFNgamma is expressed in colon in mice with minor IBD symptoms
- increased interferon gamma in the colon

abnormal interleukin level
- Il-2, but not Il-1beta is expressed in colon in mice with minor IBD symptoms
- increased IL 1 alpha, IL6, in the colon
- production of IL1 alpha is 3-4 times higher than controls 24 hours after LPS stimulation
- reduced IL4 production by irradiated CD4+ cells

abnormal iron level
- homozygotes display depleted iron stores in spleen and bone marrow

abnormal lipid level

abnormal nitric oxide homeostasis
- exhaled NO is significantly decreased

abnormal protein level
- increased phosphorylated protein kinase after insulin stimulation

abnormal tumor necrosis factor level
- increased TNF alpha in the colon
- production of TNF alpha is 3-4 times higher than controls 24 hours after LPS stimulation
- TNFalpha is expressed in colon in mice with minor IBD symptoms

decreased circulating cholesterol level
- decreased cholesterol esters

decreased circulating creatinine level

decreased circulating insulin level
- plasma insulin levels are 55% lower than controls after an overnight fast following 6 weeks on a high fat diet

decreased circulating iron level
- homozygotes display a 50% reduction in serum iron levels relative to wild-type controls

decreased physiological sensitivity to xenobiotic
- airway response to methacholine is reduced by 37%

decreased spleen iron level

enhanced wound healing
- by day 3, density of vascular structures significantly increased
- earlier and more persistent influx of greater numbers of macrophage into wound
- experimental wound is a 6 mm circular excision through the full thickness of the skin
- fully epithelialized and scab lost by 7 days
- increased collagen content and advanced maturation and organization of collagen bundles at 14 days
- macroscopic wound closure is accelerated

increased circulating cholesterol level
- increased free cholesterol

increased fatty acid level
- basal free fatty acid levels are significantly increased

increased insulin sensitivity
- greater increase in insulin stimulated whole body glucose uptake when corrected for lower plasma insulin

increased leukotriene level
- OVA-sensitized mutants exhibit higher eosinophil peroxidase and leukotriene levels in bronchoalveolar lavage fluid than wild-type mice

increased liver triglyceride level
- 54% increase in hepatic triglycerides relative to controls
- plasma triglycerides not elevated

increased myocardial infarction size
- 60% more polymorphonuclear neutrophiles per unit area in mid-ventricular slices relative to controls
- 90% more necrosis after experimental ischemia and reperfusion than found in controls

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd

digestive/alimentary phenotype

intestinal inflammation
- mice show exaggerated inflammatory response upon exposure to CML-mps-containing eluate compared to control

rectal prolapse
- 7% of mutants develop rectal prolapse at 16 weeks of age

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

homeostasis/metabolism phenotype

increased circulating interleukin-12 level
- in LPS-treated mice

increased circulating tumor necrosis factor level
- in LPS-treated mice

immune system phenotype

abnormal cytokine secretion
- 6 hours after LPS injection, TNF, Il12 and Ifng levels are substantially higher than in controls

abnormal inflammatory response
- 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
- after three subcutaneous injections of LPS into the flank, mice develop solid subcutaneous swellings whereas wild-type do not
- lesion is associated with infiltration of macrophages and neutrophils, edema, and extensive necrosis of dermal, epidermal, and muscle layers of skin
- scle layer of the skin while lesions in controls do not display edema or necrosis and show infiltration by macrophages primarily

increased circulating interleukin-12 level
- in LPS-treated mice

increased circulating tumor necrosis factor level
- in LPS-treated mice

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
- LPS-treated mice exhibit uncontrollable release of IL12 and TNF-alpha compared with wild-type mice

intestinal inflammation
- mice show exaggerated inflammatory response upon exposure to CML-mps-containing eluate compared to control

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6 * DBA/1

digestive/alimentary phenotype

colitis
- epithelial hyperplasia
- increased lymphocytes in the lamina propria
- inflamatory cells in the mucosa
- reduced mucin producing goblet cells

growth/size/body region phenotype

decreased body weight
- lower body weight than controls

immune system phenotype

colitis
- epithelial hyperplasia
- increased lymphocytes in the lamina propria
- inflamatory cells in the mucosa
- reduced mucin producing goblet cells

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * 129S/SvEv

digestive/alimentary phenotype

abnormal intestine physiology
- colonic iNOS production increases with age after 4 weeks
- ileal permeability to mannitol 3X higher than in controls at 2 weeks but normal at 6 weeks
- increased colon permeability to mannitol at 2, 4, and 10weeks but not under germ free conditions
- more IFNgamma and TNFalpha produced in the ileum and colon than in controls

colitis
- mild colitis at 4 weeks which plateaus by 8 weeks
- no colitis when raised in germ free conditions
- no ileal injury through 16 weeks

growth/size/body region phenotype

decreased body weight
- mice older than 4 weeks weigh significantly less than controls

immune system phenotype

colitis
- mild colitis at 4 weeks which plateaus by 8 weeks
- no colitis when raised in germ free conditions
- no ileal injury through 16 weeks

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
129S.Cg-Il10

cardiovascular system phenotype

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

muscle phenotype

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B10.129P2(B6)-Il10/J

immune system phenotype

decreased length of allograft survival
- acute rejection severity of cardiac allografts (BALB/c) is increased compared to wild-type controls
- decrease in survival times of heart transplants from BALB/c mice after a 30 day course of anti-CD4 and anti-CD8 mAb

The following phenotype relates to a compound genotype created using this strain

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10/J

behavior/neurological phenotype

abnormal sleep pattern
- less effect of influenza virus infection on slow wave sleep during dark phase but a greater decrease in delta wave amplitude
- lipopolysaccharide causes an overall decrease in delta wave amplitude
- lipopolysaccharide causes decreased slow wave and REM sleep during light phase
- lipopolysaccharide results in increased time spent awake, particularly in light phase
- more time in "slow-wave sleep" and less time awake during dark phase

impaired coordination
- effect persists at least 24 hours
- performance fails to improve over consecutive trials but only after IP lipopolysaccharide injection
- rotarod performance worsens after IP lipopolysaccharide injection

impaired exercise endurance
- time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment

cardiovascular system phenotype

decreased mean systemic arterial blood pressure
- lower under basal conditions

decreased susceptibility to induced choroidal neovascularization
- reduced choroidal neovascularization 7 days following krypton laser exposure of the eye

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

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
- response to endothelin 1 is eliminated in the presence of PD-98059

cellular phenotype

increased susceptibility to neuronal excitotoxicity
- increased toxicity of N-methyl-D-aspartate in primary neuron culture

digestive/alimentary phenotype

cecum inflammation
- mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice

increased colon adenocarcinoma incidence
- 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas
- tumors develop between 25 and 35 weeks of age

increased susceptibility to induced colitis
- upon DSS exposure

large intestinal inflammation
- mutants develop severe inflammation in the colon leading to inflammatory bowel disease

rectal prolapse
- rectal prolapse is seen at a median time of 16 weeks of age

growth/size/body region phenotype

slow postnatal weight gain
- lower body weight gain between 5 and 10 weeks of age than for controls

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 na¿ve CD4 T cells into immunodeficient hosts
- Normal - 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

homeostasis/metabolism phenotype

abnormal chemokine level
- LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice

abnormal cytokine level
- in LPS-injected mice
- levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment

impaired adaptive thermogenesis
- lipopolysaccharide causes a very significant drop in core body temperature

impaired exercise endurance
- time to fatigue on a motorized treadmill is reduced 24% after lipopolysaccharide treatment

increased cerebral infarction size
- lesion volume after middle cerebral artery occlusion increases 30%

increased circulating interferon-gamma level
- in LPS-injected mice

increased circulating interleukin-1 alpha level
- in LPS-injected mice

increased circulating interleukin-1 beta level
- in LPS-injected mice
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls

increased circulating interleukin-12 level
- in LPS-injected mice

increased circulating interleukin-17 level
- in LPS-injected mice

increased circulating interleukin-2 level
- in LPS-injected mice

increased circulating interleukin-6 level
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
- slightly in LPS-injected mice

increased circulating tumor necrosis factor level
- in LPS-injected mice

increased susceptibility to neuronal excitotoxicity
- increased toxicity of N-methyl-D-aspartate in primary neuron culture

immune system phenotype

abnormal chemokine level
- LPS-injected mice exhibit increased CXCL10 and CXCL1 levels compared with similarly treated wild-type mice

abnormal cytokine level
- in LPS-injected mice
- levels of cytokines increase in the brain are greater than for controls after lipopolysaccharide treatment

abnormal regulatory T cell physiology
- CD25-positive CD4 T cells from these mice fail to protect against the wasting disease induced by transferring na¿ve CD4 T cells into immunodeficient hosts
- Normal - 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

cecum inflammation
- mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice

increased circulating interferon-gamma level
- in LPS-injected mice

increased circulating interleukin-1 alpha level
- in LPS-injected mice

increased circulating interleukin-1 beta level
- in LPS-injected mice
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls

increased circulating interleukin-12 level
- in LPS-injected mice

increased circulating interleukin-17 level
- in LPS-injected mice

increased circulating interleukin-2 level
- in LPS-injected mice

increased circulating interleukin-6 level
- plasma levels remain elevated for 24 hours after lipopolysaccharide treatment as opposed to 4 hours for controls
- slightly in LPS-injected mice

increased circulating tumor necrosis factor level
- in LPS-injected mice

increased susceptibility to induced colitis
- upon DSS exposure

increased susceptibility to parasitic infection
- mice infected with T. muris exhibit increased worm burden and cecum score compared with similarly treated wild-type mice

large intestinal inflammation
- mutants develop severe inflammation in the colon leading to inflammatory bowel disease

muscle phenotype

decreased vasoconstriction
- LPS treatment markedly impairs contractions of the carotid artery induced by the thromboxane analogue U46619 and by phenylephrine

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
- response to endothelin 1 is eliminated in the presence of PD-98059

neoplasm

increased colon adenocarcinoma incidence
- 20% of mutants with colonic inflammation exhibit colon tumors; tumors are adenocarcinomas
- tumors develop between 25 and 35 weeks of age

nervous system phenotype

abnormal neuron physiology
- increased sensitivity to oxygen or glucose deprivation

increased cerebral infarction size
- lesion volume after middle cerebral artery occlusion increases 30%

increased susceptibility to neuronal excitotoxicity
- increased toxicity of N-methyl-D-aspartate in primary neuron culture

vision/eye phenotype

decreased susceptibility to induced choroidal neovascularization
- reduced choroidal neovascularization 7 days following krypton laser exposure of the eye

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10

homeostasis/metabolism phenotype

abnormal circulating interleukin-12b level
- PGE2 represses LPS induction to a lesser extent than it does in controls

abnormal circulating interleukin-6 level
- PGE2 represses LPS induction to a lesser extent than it does in controls

immune system phenotype

abnormal circulating interleukin-12b level
- PGE2 represses LPS induction to a lesser extent than it does in controls

abnormal circulating interleukin-6 level
- PGE2 represses LPS induction to a lesser extent than it does in controls

References

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

Additional References

Nikoopour E; Lin CM; Sheskey S; Heckenlively JR; Lundy SK. 2019. Immune Cell Infiltration into the Eye Is Controlled by IL-10 in Recoverin-Induced Autoimmune Retinopathy. J Immunol 202(4):1057-1068PubMed: 30635390 MGI: J:272976
Giannakopoulou CE; Sotiriou A; Dettoraki M; Yang M; Perlikos F; Toumpanakis D; Prezerakos G; Koutsourelakis I; Kastis GA; Vassilakopoulou V; Mizi E; Papalois A; Greer JJ; Vassilakopoulos T. 2019. Regulation of breathing pattern by IL-10. Am J Physiol Regul Integr Comp Physiol 317(1):R190-R202PubMed: 31091151 MGI: J:276946
Nandula SR; Dey P; Corbin KL; Nunemaker CS; Bagavant H; Deshmukh US. 2013. Salivary gland hypofunction induced by activation of innate immunity is dependent on type I interferon signaling. J Oral Pathol Med 42(1):66-72PubMed: 22672212 MGI: J:279149
Berg DJ; Davidson N; Kuhn R; Muller W; Menon S; Holland G; Thompson-Snipes L; Leach MW; Rennick D. 1996. Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses. J Clin Invest 98(4):1010-20PubMed: 8770874 MGI: J:35020
Justice JP; Shibata Y; Sur S; Mustafa J; Fan M; Van Scott MR. 2001. IL-10 gene knockout attenuates allergen-induced airway hyperresponsiveness in C57BL/6 mice. Am J Physiol Lung Cell Mol Physiol 280(2):L363-8PubMed: 11159016 MGI: J:68061
O'Mahony L; Feeney M; O'Halloran S; Murphy L; Kiely B; Fitzgibbon J; Lee G; O'Sullivan G; Shanahan F; Collins JK. 2001. Probiotic impact on microbial flora, inflammation and tumour development in IL-10 knockout mice. Aliment Pharmacol Ther 15(8):1219-25PubMed: 11472326 MGI: J:70926
Wang Q; Fang CH; Hasselgren PO. 2001. Intestinal permeability is reduced and IL-10 levels are increased in septic IL-6 knockout mice. Am J Physiol Regul Integr Comp Physiol 281(3):R1013-23PubMed: 11507020 MGI: J:71507
Murphy ML; Wille U; Villegas EN; Hunter CA; Farrell JP. 2001. IL-10 mediates susceptibility to Leishmania donovani infection. Eur J Immunol 31(10):2848-56PubMed: 11592059 MGI: J:72355
Pimenta-Araujo R; Mascarell L; Huesca M; Cumano A; Bandeira A. 2002. Deoxyguanosine blocks allograft rejection of thymic epithelium but not lymphocyte infiltration and recognition. Eur J Immunol 32(1):77-86PubMed: 11754006 MGI: J:73937
Mizoguchi A; Mizoguchi E; Takedatsu H; Blumberg RS; Bhan AK. 2002. Chronic Intestinal Inflammatory Condition Generates IL-10-Producing Regulatory B Cell Subset Characterized by CD1d Upregulation. Immunity 16(2):219-30PubMed: 11869683 MGI: J:74718
Teshima T; Reddy P; Lowler KP; KuKuruga MA; Liu C; Cooke KR; Ferrara JL. 2002. Flt3 ligand therapy for recipients of allogeneic bone marrow transplants expands host CD8 alpha(+) dendritic cells and reduces experimental acute graft-versus-host disease. Blood 99(5):1825-32PubMed: 11861301 MGI: J:75083
Rachmilewitz D; Karmeli F; Takabayashi K; Hayashi T; Leider-Trejo L; Lee J; Leoni LM; Raz E. 2002. Immunostimulatory DNA ameliorates experimental and spontaneous murine colitis. Gastroenterology 122(5):1428-41PubMed: 11984528 MGI: J:76343
Huang EH; Carter JJ; Whelan RL; Liu YH; Rosenberg JO; Rotterdam H; Schmidt AM; Stern DM; Forde KA. 2002. Colonoscopy in mice. Surg Endosc 16(1):22-4PubMed: 11961598 MGI: J:77864
Yin Z; Bahtiyar G; Zhang N; Liu L; Zhu P; Robert ME; McNiff J; Madaio MP; Craft J. 2002. IL-10 regulates murine lupus. J Immunol 169(4):2148-55PubMed: 12165544 MGI: J:78239
Das G; Augustine MM; Das J; Bottomly K; Ray P; Ray A. 2003. An important regulatory role for CD4+CD8 alpha alpha T cells in the intestinal epithelial layer in the prevention of inflammatory bowel disease. Proc Natl Acad Sci U S A 100(9):5324-9PubMed: 12695566 MGI: J:83283
Hegazi RA; Mady HH; Melhem MF; Sepulveda AR; Mohi M; Kandil HM. 2003. Celecoxib and rofecoxib potentiate chronic colitis and premalignant changes in interleukin 10 knockout mice. Inflamm Bowel Dis 9(4):230-6PubMed: 12902846 MGI: J:85702
Bernert H; Sekikawa K; Radcliffe RA; Iraqi F; You M; Malkinson AM. 2003. Tnfa and Il-10 deficiencies have contrasting effects on lung tumor susceptibility: Gender-dependent modulation of IL-10 haploinsufficiency. Mol Carcinog 38(3):117-23PubMed: 14587096 MGI: J:86489
Froicu M; Weaver V; Wynn TA; McDowell MA; Welsh JE; Cantorna MT. 2003. A crucial role for the vitamin d receptor in experimental inflammatory bowel diseases. Mol Endocrinol 17(12):2386-92PubMed: 14500760 MGI: J:86860
Morrison AC; Wilson CB; Ray M; Correll PH. 2004. Macrophage-stimulating protein, the ligand for the stem cell-derived tyrosine kinase/RON receptor tyrosine kinase, inhibits IL-12 production by primary peritoneal macrophages stimulated with IFN-gamma and lipopolysaccharide. J Immunol 172(3):1825-32PubMed: 14734766 MGI: J:87661
Lin T; Bost KL. 2004. STAT3 activation in macrophages following infection with Salmonella. Biochem Biophys Res Commun 321(4):828-34PubMed: 15358102 MGI: J:91740
Dresner-Pollak R; Gelb N; Rachmilewitz D; Karmeli F; Weinreb M. 2004. Interleukin 10-deficient mice develop osteopenia, decreased bone formation, and mechanical fragility of long bones. Gastroenterology 127(3):792-801PubMed: 15362035 MGI: J:93577

Additional - Il10^tm1Cgn related

Technical Support

Contact Technical Support

Genotyping Protocols
- Standard PCR:Il10^tm1Cgn
- Standard PCR:Il10^tm1Cgn
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a good breeder.

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.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Appearance
- black
  Related Genotype: a/a
Citation
When using the Il-10 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #002251 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

RB16 (Maximum)

Pricing & Availability

Available Now

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous for Il10<tm1Cgn>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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.

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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.

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"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"). "PRODUCT(S)" means biological materials supplied by JACKSON, and their derivatives. "SERVICES" means projects conducted by JACKSON for other parties that may include but are not limited to the use of MICE or PRODUCTS. "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 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, PRODUCTS or SERVICES from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON’s prior written authorization.

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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.

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Also Known As: Il-10 KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Il10tm1Cgn

Allele Symbol: Il10tm1Cgn

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Genotype

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

Genotype: Il10tm1Cgn related

Mammalian Phenotype Terms by Genotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd * C57BL/6

behavior/neurological phenotype

craniofacial phenotype

immune system phenotype

digestive/alimentary phenotype

integument phenotype

limbs/digits/tail phenotype

liver/biliary system phenotype

mammalian phenotype

mortality/aging

neoplasm

respiratory system phenotype

skeleton phenotype

cardiovascular system phenotype

embryo phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hematopoietic system phenotype

cellular phenotype

homeostasis/metabolism phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd

digestive/alimentary phenotype

reproductive system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd * C57BL/6 * DBA/1

digestive/alimentary phenotype

growth/size/body region phenotype

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgninvolves: 129P2/OlaHsd * 129S/SvEv

digestive/alimentary phenotype

growth/size/body region phenotype

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1Cgn129S.Cg-Il10

cardiovascular system phenotype

muscle phenotype

Genotype: Il10tm1Cgn/Il10tm1CgnB10.129P2(B6)-Il10/J

immune system phenotype

Genotype: Il10tm1Cgn/Il10tm1CgnB6.129P2-Il10/J

behavior/neurological phenotype

cardiovascular system phenotype

cellular phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

muscle phenotype

neoplasm

nervous system phenotype

vision/eye phenotype

Genotype: Il10tm1Cgn/Il10tm1CgnB6.129P2-Il10

homeostasis/metabolism phenotype

immune system phenotype

References

Additional References

Additional - Il10tm1Cgn related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Il10^tm1Cgn

Allele Symbol: Il10^tm1Cgn

Genotype: Il10^tm1Cgn related

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * C57BL/6 * DBA/1

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
involves: 129P2/OlaHsd * 129S/SvEv

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
129S.Cg-Il10

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B10.129P2(B6)-Il10/J

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10/J

Genotype: Il10^tm1Cgn/Il10^tm1Cgn
B6.129P2-Il10

Additional - Il10^tm1Cgn related