Phenotypes associated with this allele

• Allele Symbol: Icam1^tm1Jcgr
• Allele Name: targeted mutation 1, Jose Carlos Gutierrez Ramos
• Allele ID: MGI:1857292
• Summary: 8 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Icam1^tm1Jcgr/Icam1^tm1Jcgr	B6.129S4-Icam1^tm1Jcgr	MGI:3785286
hm2	Icam1^tm1Jcgr/Icam1^tm1Jcgr	B6.129S4-Icam1^tm1Jcgr/J	MGI:3688529
hm3	Icam1^tm1Jcgr/Icam1^tm1Jcgr	involves: 129S4/SvJae * C57BL/6 * DBA/2	MGI:2179067
cx4	Icam1^tm1Jcgr/Icam1^tm1Jcgr Ldlr^tm1Her/Ldlr^tm1Her	involves: 129S4/SvJae * 129S7/SvEvBrd	MGI:3620575
cx5	Icam1^tm1Jcgr/Icam1^tm1Jcgr Ldlr^tm1Her/Ldlr^tm1Her Vcam1^tm1Dmil/Vcam1^tm1Dmil	involves: 129S4/SvJae * 129S7/SvEvBrd * C57BL/6	MGI:3620574
cx6	Icam1^tm1Jcgr/Icam1^tm1Jcgr Vcam1^tm1Dmil/Vcam1^tm1Dmil	involves: 129S4/SvJae * C57BL/6	MGI:5701417
cx7	Icam1^tm1Jcgr/Icam1^tm1Jcgr Vcam1^tm1Dmil/Vcam1^+	involves: 129S4/SvJae * C57BL/6	MGI:5701418
cx8	Icam1^tm1Jcgr/Icam1^tm1Jcgr Tg(INS-Il10)#Sar/0	NOD.Cg-Icam1^tm1Jcgr Tg(INS-Il10)#Sar	MGI:3622779

Genotype
MGI:3785286

hm1

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr
• Genetic Background: B6.129S4-Icam1^tm1Jcgr

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

immune system

immune system phenotype ( J:113463 )

N • mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis

Genotype
MGI:3688529

hm2

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr
• Genetic Background: B6.129S4-Icam1^tm1Jcgr/J

cardiovascular system

abnormal cardiac muscle contractility ( J:114093 )

• 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

muscle

abnormal cardiac muscle contractility ( J:114093 )

• 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

Genotype
MGI:2179067

hm3

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * DBA/2

mortality/aging

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:18743 )

• 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)

immune system

increased neutrophil cell number ( J:18743 )

• significant elevation in circulating neutrophils

increased lymphocyte cell number ( J:18743 )

• significant elevation in circulating lymphocytes

abnormal T cell physiology ( J:18743 )

• T cells are diminished in their ability to stimulate an allogeneic response

abnormal interleukin level ( J:18743 )

• 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

abnormal tumor necrosis factor level ( J:18743 )

• 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

decreased susceptibility to type IV hypersensitivity reaction ( J:18743 )

• reduction in contact hypersensitivity response

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:18743 )

• 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)

hematopoietic system

increased neutrophil cell number ( J:18743 )

• significant elevation in circulating neutrophils

increased lymphocyte cell number ( J:18743 )

• significant elevation in circulating lymphocytes

abnormal T cell physiology ( J:18743 )

• T cells are diminished in their ability to stimulate an allogeneic response

homeostasis/metabolism

abnormal interleukin level ( J:18743 )

• 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

abnormal tumor necrosis factor level ( J:18743 )

• 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

Genotype
MGI:3620575

cx4

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr; Ldlr^tm1Her/Ldlr^tm1Her
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd

hematopoietic system

increased neutrophil cell number ( J:69597 )

• 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

immune system

increased neutrophil cell number ( J:69597 )

• 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

Genotype
MGI:3620574

cx5

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr; Ldlr^tm1Her/Ldlr^tm1Her; Vcam1^tm1Dmil/Vcam1^tm1Dmil
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd * C57BL/6

cardiovascular system

decreased susceptibility to atherosclerosis ( J:69597 )

• 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

homeostasis/metabolism

decreased circulating cholesterol level ( J:69597 )

• after an 8-week cholesterol-enriched diet, develop a less severe hypercholesterolemia than single homozygous Ldlr mutant mice

immune system

increased leukocyte cell number ( J:69597 )

• total leukocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

increased neutrophil cell number ( J:69597 )

• neutrophil counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

increased lymphocyte cell number ( J:69597 )

• lymphocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

increased monocyte cell number ( J:69597 )

• monocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

hematopoietic system

increased leukocyte cell number ( J:69597 )

• total leukocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

increased neutrophil cell number ( J:69597 )

• neutrophil counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

increased lymphocyte cell number ( J:69597 )

• lymphocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

increased monocyte cell number ( J:69597 )

• monocyte counts are increased when mice have been on an 8-week cholesterol-enriched diet compared to homozygous Ldlr mutant mice

Genotype
MGI:5701417

cx6

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr; Vcam1^tm1Dmil/Vcam1^tm1Dmil
• Genetic Background: involves: 129S4/SvJae * C57BL/6

cellular

impaired macrophage chemotaxis ( J:227109 )

• reduced recruitment of monocytes/macrophages into peritoneal cavity as compared to wild-type following IP challenge with thioglycollate

decreased cell chemotaxis ( J:227109 )

• reduced recruitment of leukocytes into peritoneal cavity as compared to wild-type and heterozygous Vcam1^tmDmil following IP challenge with ovalbumin

• numbers of monocytes, macrophages and lymphocytes recovered from the peritoneal cavity are reduced, but not neutrophils or eosinophils

hematopoietic system

impaired macrophage chemotaxis ( J:227109 )

• reduced recruitment of monocytes/macrophages into peritoneal cavity as compared to wild-type following IP challenge with thioglycollate

immune system

impaired macrophage chemotaxis ( J:227109 )

• reduced recruitment of monocytes/macrophages into peritoneal cavity as compared to wild-type following IP challenge with thioglycollate

Genotype
MGI:5701418

cx7

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr; Vcam1^tm1Dmil/Vcam1⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

cellular

decreased cell chemotaxis ( J:227109 )

• 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

Genotype
MGI:3622779

cx8

• Allelic Composition: Icam1^tm1Jcgr/Icam1^tm1Jcgr; Tg(INS-Il10)#Sar/0
• Genetic Background: NOD.Cg-Icam1^tm1Jcgr Tg(INS-Il10)#Sar

immune system

periinsulitis ( J:66103 )

• ICAM-I deficient transgenic mice develop periinsulitis but not insulitis as do wild-type transgenic NOD mice

decreased susceptibility to autoimmune diabetes ( J:66103 )

• 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

endocrine/exocrine glands

periinsulitis ( J:66103 )

• ICAM-I deficient transgenic mice develop periinsulitis but not insulitis as do wild-type transgenic NOD mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
NOT	type 1 diabetes mellitus	DOID:9744	OMIM:222100	J:98583