Analysis Tools
immune system
| N |
• mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis
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Allele Symbol Allele Name Allele ID |
Icam1tm1Jcgr targeted mutation 1, Jose Carlos Gutierrez Ramos MGI:1857292 |
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| Summary |
8 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• lipopolysaccharide (LPS) treatment does not result in a decrease in left ventricular contractility as is seen in wild-type, indicating a lack of LPS-induced myocardial dysfunction
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• lipopolysaccharide (LPS) treatment does not result in a decrease in left ventricular contractility as is seen in wild-type, indicating a lack of LPS-induced myocardial dysfunction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• resistant to the lethal effect of high doses of endotoxin (LPS) but do not show a decrease in the production of TNF-alpha and IL-1
• D-Gal-sensitized mice are resistant to the lethal effects of low doses of exotoxin (SEB) but not to low doses of endotoxin (LPS)
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• significant elevation in circulating neutrophils
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• significant elevation in circulating lymphocytes
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• T cells are diminished in their ability to stimulate an allogeneic response
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• D-Gal-sensitized mice challenged with exotoxin (SEB), but not endotoxin (LPS), show more than 50% reduction in IL-1 levels 90 min after treatment and sustain lower levels for up to 8 hours
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• D-Gal-sensitized mice challenged with exotoxin (SEB), but not endotoxin (LPS), show more than 50% reduction in TNF-alpha levels 90 min after treatment and sustain lower levels for up to 8 hours
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• reduction in contact hypersensitivity response
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• resistant to the lethal effect of high doses of endotoxin (LPS) but do not show a decrease in the production of TNF-alpha and IL-1
• D-Gal-sensitized mice are resistant to the lethal effects of low doses of exotoxin (SEB) but not to low doses of endotoxin (LPS)
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• significant elevation in circulating neutrophils
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• significant elevation in circulating lymphocytes
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• T cells are diminished in their ability to stimulate an allogeneic response
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• D-Gal-sensitized mice challenged with exotoxin (SEB), but not endotoxin (LPS), show more than 50% reduction in IL-1 levels 90 min after treatment and sustain lower levels for up to 8 hours
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• D-Gal-sensitized mice challenged with exotoxin (SEB), but not endotoxin (LPS), show more than 50% reduction in TNF-alpha levels 90 min after treatment and sustain lower levels for up to 8 hours
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• neutrophil counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mice, however develop aortic lesions to the same extent as homozygous Ldlr mice
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• neutrophil counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mice, however develop aortic lesions to the same extent as homozygous Ldlr mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after an 8-week cholesterol-enriched diet, whole aorta and arch lesion area is reduced by 31% and 45%, respectively, compared to double homozygous Icam1 and Ldlr mice, and by 48% and 38%, respectively, compared to single homozygous Ldlr mutant mice
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• after an 8-week cholesterol-enriched diet, develop a less severe hypercholesterolemia than single homozygous Ldlr mutant mice
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• total leukocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• neutrophil counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• lymphocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• monocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• total leukocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• neutrophil counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• lymphocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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• monocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced recruitment of monocytes/macrophages into peritoneal cavity as compared to wild-type following IP challenge with thioglycollate
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• reduced recruitment of leukocytes into peritoneal cavity as compared to wild-type and heterozygous Vcam1tmDmil following IP challenge with ovalbumin
• numbers of monocytes, macrophages and lymphocytes recovered from the peritoneal cavity are reduced, but not neutrophils or eosinophils
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• reduced recruitment of monocytes/macrophages into peritoneal cavity as compared to wild-type following IP challenge with thioglycollate
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• reduced recruitment of monocytes/macrophages into peritoneal cavity as compared to wild-type following IP challenge with thioglycollate
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced recruitment of leukocytes into peritoneal cavity as compared to wild-type, but not homozygote, following IP challenge with ovalbumin
• numbers of monocytes, macrophages and lymphocytes recovered from the peritoneal cavity are reduced, but not neutrophils or eosinophils
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• ICAM-I deficient transgenic mice develop periinsulitis but not insulitis as do wild-type transgenic NOD mice
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• wild-type transgenic NOD mice readily develop diabetes starting at 5 weeks (blood glucose >300 mg/dl), while ICAM-I deficient transgenic NOD mice have not developed diabetes at 12 weeks (n=4) or 16 weeks (n=5); nontransgenic ICAM-I deficient mice do not develop diabetes over the same period
• transfer of concanavalin A treated splenocytes from 8 week old Tg(TcraBDC2.5)1Doi Tg(TcraBDC2.5)1Doi female mice expressing an islet-specific TCR transgene to irradiated ICAM-I deficient NOD or deficient transgenic NOD mice does not induce diabetes in recipients
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• ICAM-I deficient transgenic mice develop periinsulitis but not insulitis as do wild-type transgenic NOD mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| NOT | type 1 diabetes mellitus | DOID:9744 |
OMIM:222100 |
J:98583 |
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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