Analysis Tools
immune system
| N |
• mice co-housed with wild-type mice do not affect the susceptibility to induced colitis of wild-type mice
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Allele Symbol Allele Name Allele ID |
Il1r1tm1Imx targeted mutation 1, Immunex Research and Development Corporation MGI:1861112 |
| Summary |
12 genotypes |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice co-housed with wild-type mice do not affect the susceptibility to induced colitis of wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following S. aureus infection
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• 96 hours following S. aureus infection
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• 24 hours following S. aureus infection
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• 96 hours following S. aureus infection
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• 4 and 24 hours following S. aureus infection
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• in spleen cells stimulated with formalin-killed S. aureus infection for 48 hours
(J:125570)
• within wound fluids on days 1, 3, 5, 10, and 14 of wound healing
(J:148779)
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• in spleen cells stimulated with formalin-killed S. aureus infection
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• following S. aureus infection
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• following S. aureus infection, mice exhibit severe septicemia, increased weight loss, increased frequency and severity of arthritis, increased bacterial load, and decreased survival compared with wild-type mice
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• following S. aureus infection
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• following carotid ligation, mice exhibit a 19-fold reduction in neointima/media area, 3.4-fold increase in lumen area, and decrease in total vessel area compared with wild-type mice
• neointima formation following carotid ligation is disrupted to a greater extent when null mice transplanted with null bone marrow compared when null mice are receive wild-type bone marrow or wild-type mice receive null bone marrow
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• 2-fold in 9 and 11 month old mice
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• in older mice
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• 2-fold in 9 and 11 month old mice
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• 96 hours following S. aureus infection
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• 24 hours following S. aureus infection
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• 96 hours following S. aureus infection
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• 4 and 24 hours following S. aureus infection
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• during the first half of the dark cycle
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• following glucose challenge, older mice exhibit impaired plasma glucose elimination compared with wild-type mice
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• in older mice
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• within wound fluids on day 1 of wound healing
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• after wound healing, mice exhibit decreased scar width and depth compared with wild-type mice
• deep tissue wounds exhibit 3-fold less fibrosis compared to in wild-type mice
• however, mice exhibit normal cellular infiltration and tensile strength of skin wounds
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• in older mice
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• older mice exhibit a decrease in percentage lean body mass but an increase in absolute lean body mass compared with wild-type mice
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• following S. aureus infection
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• after 5 to 6 months
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• in older mice
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• in older mice
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• in older mice
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• 2-fold at 9 months of age
• however, mice exhibit normal body fat at 4 months of age
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• in older mice
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• in older mice
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• in older mice
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• in older mice
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• at 19 months, intra-abdominal fat mass is increased 1.5- to 1.7-fold compared with wild-type mice
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• in older mice
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• following S. aureus infection
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• preobese mice exhibit mild leptin resistance compared with wild-type mice
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• mice exhibit reduced latency to drink in a novelty-induced hypophagia test compared with wild-type mice
• mice spend more time in the open arms of an elevated plus maze compared with wild-type mice
• mice exhibit increased latency to enter into the dark chamber in a light/dark test compared with wild-type mice
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• during the dark phase at 4 months
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• in older mice
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• following carotid ligation, mice exhibit a 19-fold reduction in neointima/media area, 3.4-fold increase in lumen area, and decrease in total vessel area compared with wild-type mice
• neointima formation following carotid ligation is disrupted to a greater extent when null mice transplanted with null bone marrow compared when null mice are receive wild-type bone marrow or wild-type mice receive null bone marrow
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• following administration of kainate, Purkinje cells fail to exhibit an increase in firing rate unlike wild-type cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• no IL-6 is detected in sera of mice injected with IL-1alpha
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• no IL-6 is detected in sera of mice injected with IL-1alpha
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• osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp
• the osteolytic lesions continue to be larger for at least 38 days post inoculation
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• mice have 3 log greater bacterial penetration of the dental pulp eight days after bacterial innoculation
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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• osteolytic lesions of molars are significantly larger in these mice 2 weeks after bacterial inoculation of the dental pulp
• the osteolytic lesions continue to be larger for at least 38 days post inoculation
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• there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp
• osteoclast activity of the molars is 2-fold higher than in wild-types 7 days after bacterial inoculation
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 21 days after inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit delayed eruption of mandibular and maxillary incisors and molars compared with wild-type mice
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• neutrophile response to monosodium urate injected into the peritoneal cavity is reduced 85% relative to controls
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• neutrophile response to monosodium urate injected into the peritoneal cavity is reduced 85% relative to controls
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• mice exhibit delayed eruption of mandibular and maxillary incisors and molars compared with wild-type mice
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• mice exhibit delayed eruption of mandibular and maxillary incisors and molars compared with wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following ischemic/reperfusion injury, mice exhibit reduced serum creatinine levels at 48 and 72 hours compared with wild-type mice
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• following ischemic/reperfusion injury, mice exhibit reduced blood urea nitrogen levels at 48 and 72 hours compared with wild-type mice
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• mice treated with IL1b, either intraperitoneally or intracerebroventricularly, fail to exhibit a decrease in social exploration, immobility, decrease in body weight, or reduced food intake compared with similarly treated wild-type mice
• pretreatment with TNFbp attenuates depressive effect of LPS unlike in similarly treated wild-type mice
• however, behavioral response to LPS treatment is normal
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• following ischemic/reperfusion injury, mice exhibit reduced blood urea nitrogen and creatinine levels at 48 and 72 hours with reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
• however, tubular damage is normal
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• following ischemic/reperfusion injury, mice exhibit reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
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• following reverse passive Arthus reaction to induce uveitis, mice exhibit reduced cellular infiltration into the anterior and posterior segments compared with wild-type mice
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• following ischemic/reperfusion injury, mice exhibit reduced blood urea nitrogen and creatinine levels at 48 and 72 hours with reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
• however, tubular damage is normal
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• in some experiments
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• following ischemic/reperfusion injury, mice exhibit reduced polymorphonuclear leukocyte infiltration compared with wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• when fed a Western diet with high cholate, but not when fed standard chow or a Western diet
• mice receiving Apoetm1Unc bone marrow develop 1.9-fold smaller lesions compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet or a Western diet with high cholate compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet with high cholate, mice exhibit a greater active pressure-diameter response compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes
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• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• during the last 6 hours of the dark period, mice exhibit increased awake time and less non-REM sleep compared with wild-type mice wild-type mice
• during the light period, mice exhibit fewer bouts of REM sleep compared with wild-type mice
• following sleep deprivation, mice fail to exhibit REM sleep rebound unlike wild-type mice and exhibit more time awake and less time in non-REM sleep during the first 6 hours of dark period compared with wild-type mice
• however, the length of REM sleep bouts is normal
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• brain temperature during the dark phase is higher than in wild-type mice
• mice exhibit lower brain temperature during the first 6 hours following sleep deprivation compared with wild-type mice
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• mice exhibit a greater contribution of slower frequencies to the total power of the non-REM sleep power spectra, measured by electrocorticogram, compared with wild-type mice
• theta power contributes less to total power compared to in wild-type mice
• following sleep deprivation, mice exhibit higher delta power compared with wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• DSS-treated mice exhibit more severe colitis compared with wild-type mice and Vsig4tm1Gne homozygotes
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• in MOG35-55 treated mice
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• in MOG35-55 treated mice
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• MOG35-55 treated mice exhibit delayed onset and reduced clinical score, reduced leukocyte spinal cord infiltration, and decreased TH1 and TH17 cells in the spinal cord and spleen compared with wild-type mice and Vsig4tm1Gne homozygotes
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• DSS-treated mice exhibit more severe colitis compared with wild-type mice and Vsig4tm1Gne homozygotes
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• in MOG35-55 treated mice
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• in MOG35-55 treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• resistance to endotoxin shock induced by high dose lipopolysaccharide (LPS)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• inflammation damages the tear-secreting acinar cells and interlobular septa
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• progresses from desiccation and keratinization of the ocular surface
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• desiccation and keratinization of the ocular surface
• ocular surface epitheliopathy
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• inflammation damages the tear-secreting acinar cells and interlobular septa
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• mice exhibit an increase in acidified conjunctival goblet cells compared with wild-type mice
• however, the total number of goblet cells is normal
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• ocular mucosal epithelia metaplasia
• squamous metaplasia
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• inflammation damages the tear-secreting acinar cells and interlobular septa
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• inflammation damages the tear-secreting acinar cells and interlobular septa
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• inflammation damages the tear-secreting acinar cells and interlobular septa
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Sjogren's syndrome | DOID:12894 |
OMIM:270150 |
J:163691 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mostly CD4+ T cells
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• mice exhibit an increase in acidified conjunctival goblet cells compared with wild-type mice that is not as severe as in Airetm1.1Doi homozygotes
• however, the total number of goblet cells is normal
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• mice exhibit ocular mucosal epithelia metaplasia and ocular surface epitheliopathy that is not as severe as in Airetm1.1Doi homozygotes
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• progresses from desiccation and keratinization of the ocular surface
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• mostly CD4+ T cells
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• mostly CD4+ T cells
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Sjogren's syndrome | DOID:12894 |
OMIM:270150 |
J:163691 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• lungs infected with E. coli have decreased amounts of neutrophils that emigrate from the alveolar septae
• neutrophil numbers in circulation or sequestered within the alveolar septae are similar to wild-type
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• there is 2-fold less levels of Cxcl1 (KC) found in the bronchoalveolar lavage fluid of lungs infected with E. coli compared to infected wild-type mice
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• into the aqueous humor following induction of uveitis
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• following reverse passive Arthus reaction to induce uveitis, mice exhibit reduced cellular infiltration into the anterior and posterior segments and IL6 secretion into the aqueous humor compared with wild-type mice
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• osteolytic lesions of molars are larger in these mice 2 weeks after bacterial inoculation of the dental pulp compared to either wild-type controls or to homozygotes that are null for just one gene
• the osteolytic lesions continue to be larger for at least 38 days after inoculation
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• patchy pulmonary inflammation occurs spontaneously in about 2/3rd of mice
• infiltrates contain mixed populations of leukocytes and are localized to the pleura, subpleura alveoli, and perivascular tissue
• eosinophilic crystalline deposits are found in the alveolar air spaces of inflamed areas
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• lungs with pneumonia induced by E. coli inoculation have less neutrophil migration into the alveolar air spaces and less accumulation of extravascular plasma
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• mice have 4 log greater bacterial penetration of the dental pulp eight days after experimental bacterial infection
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 7 days after bacterial inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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• osteolytic lesions of molars are larger in these mice 2 weeks after bacterial inoculation of the dental pulp compared to either wild-type controls or to homozygotes that are null for just one gene
• the osteolytic lesions continue to be larger for at least 38 days after inoculation
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• there is significantly more osteoclastogenesis that occurs in molars between 7 and 21 days after bacterial infection of the dental pulp
• osteoclast activity of the molars is 5-fold higher than in wild-types 7 days after bacterial inoculation
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• patchy pulmonary inflammation occurs spontaneously in about 2/3rd of mice
• infiltrates contain mixed populations of leukocytes and are localized to the pleura, subpleura alveoli, and perivascular tissue
• eosinophilic crystalline deposits are found in the alveolar air spaces of inflamed areas
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• lungs with pneumonia induced by E. coli inoculation have less neutrophil migration into the alveolar air spaces and less accumulation of extravascular plasma
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• there is 2-fold less levels of Cxcl1 (KC) found in the bronchoalveolar lavage fluid of lungs infected with E. coli compared to infected wild-type mice
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• lungs infected with E. coli have decreased amounts of neutrophils that emigrate from the alveolar septae
• neutrophil numbers in circulation or sequestered within the alveolar septae are similar to wild-type
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 7 days after bacterial inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 7 days after bacterial inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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• mice have significantly higher necrosis scores of the dental pulp seven days after bacterial inoculation
• complete necrosis of the dental pulp is observed by 7 days after bacterial inoculation compared to control mice that still have intact dental pulp at 38 days post-innoculation
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/23/2024 MGI 6.23 |
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