Phenotypes associated with this allele

• Allele Symbol: Icam1^tm1Bay
• Allele Name: targeted mutation 1, Baylor College of Medicine
• Allele ID: MGI:1857183
• Summary: 10 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Icam1^tm1Bay/Icam1^tm1Bay	B6.129S7-Icam1^tm1Bay	MGI:3606606
hm2	Icam1^tm1Bay/Icam1^tm1Bay	B6.129S7-Icam1^tm1Bay/J	MGI:3766730
hm3	Icam1^tm1Bay/Icam1^tm1Bay	either: B6.129S7-Icam1^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)	MGI:3766601
hm4	Icam1^tm1Bay/Icam1^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:3766946
hm5	Icam1^tm1Bay/Icam1^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6J	MGI:2179060
cx6	Icam1^tm1Bay/Icam1^tm1Bay Sell^tm1Tft/Sell^tm1Tft	B6.129-Sell^tm1Tft Icam1^tm1Bay	MGI:3766625
cx7	Icam1^tm1Bay/Icam1^tm1Bay Selp^tm1Bay/Selp^tm1Bay	B6.129S7-Icam1^tm1Bay Selp^tm1Bay/J	MGI:3767011
cx8	Icam1^tm1Bay/Icam1^tm1Bay Selp^tm1Bay/Selp^tm1Bay	either: B6.129S7-Selp^tm1Bay Icam1^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)	MGI:3766607
cx9	Icam1^tm1Bay/Icam1^tm1Bay Sele^tm2Alb/Sele^tm2Alb Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:3766947
cx10	Icam1^tm1Bay/Icam1^tm1Bay Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3606608

Genotype
MGI:3606606

hm1

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay
• Genetic Background: B6.129S7-Icam1^tm1Bay

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

growth/size/body

increased body weight ( J:48271 )

• mice are ~20% heavier than wild-type or Sell^tm1Tft mutant mice

immune system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 64% after 4 hours

abnormal cellular extravasation ( J:48271 )

• 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 61% compared to wild-type

abnormal leukocyte tethering or rolling ( J:48271 )

• Tnfa (TNFalpha) treatment increases leukocyte rolling flux fraction slightly compared to wild-type

• rolling velocities of leukocytes are slightly greater compared to wild-type mice at times <30 minutes after surgery; >60 minutes after surgery-induced inflammation, rolling velocities are significantly faster than wild-type (58 vs 38 um/second)

• similar results on rolling velocity are observed with Tnfa-activated rolling as induced by surgical trauma

increased eosinophil cell number ( J:48271 )

• increased significantly compared to wild-type (178% of wild-type)

increased neutrophil cell number ( J:24239 , J:48271 )

• 4-5 fold increase in numbers of circulating neutrophils (J:24239)

• number of circulating neutrophils is increased over wild-type (190% of wild-type number) (J:48271)

increased lymphocyte cell number ( J:48271 )

• number of circulating lymphocytes is increased over wild-type (47% of wild-type number)

increased monocyte cell number ( J:48271 )

• number of circulating monocytes is increased over wild-type (223% of wild-type number)

decreased susceptibility to endotoxin shock ( J:123460 )

• following treatment with a lethal dose of LPS, mice succumb after 10 hours compared to wild-type mice that succumb after 8 hours

• mice only develop mild liver injury in response to low doses of LPS at 8 hours that does not worsen compared to wild-type mice that exhibit liver severe injury at 6 hours

hematopoietic system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 64% after 4 hours

abnormal cellular extravasation ( J:48271 )

• 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 61% compared to wild-type

abnormal leukocyte tethering or rolling ( J:48271 )

• Tnfa (TNFalpha) treatment increases leukocyte rolling flux fraction slightly compared to wild-type

• rolling velocities of leukocytes are slightly greater compared to wild-type mice at times <30 minutes after surgery; >60 minutes after surgery-induced inflammation, rolling velocities are significantly faster than wild-type (58 vs 38 um/second)

• similar results on rolling velocity are observed with Tnfa-activated rolling as induced by surgical trauma

increased eosinophil cell number ( J:48271 )

• increased significantly compared to wild-type (178% of wild-type)

increased neutrophil cell number ( J:24239 , J:48271 )

• 4-5 fold increase in numbers of circulating neutrophils (J:24239)

• number of circulating neutrophils is increased over wild-type (190% of wild-type number) (J:48271)

increased lymphocyte cell number ( J:48271 )

• number of circulating lymphocytes is increased over wild-type (47% of wild-type number)

increased monocyte cell number ( J:48271 )

• number of circulating monocytes is increased over wild-type (223% of wild-type number)

neoplasm

increased tumor growth/size ( J:108135 )

• when injected with melanoma cells, mice exhibit a 2.6 fold increase in tumor volume on day 14 compared to wild-type mice

cardiovascular system

decreased angiogenesis ( J:118196 )

• in a disk angiogenesis assay, no increase in capillary density in response to Vegfa is observed in the dermal vasculature overlying implanted disks, whereas wild-type mice show a clear increase in capillary density in response to Vegfa

cellular

abnormal cell physiology ( J:118196 )

• endothelial cells show attenuated chemotactic response to Vegfa in transwell chemotactic assays compared with wild-type control cells

abnormal cell migration ( J:118196 )

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 64% after 4 hours

abnormal cellular extravasation ( J:48271 )

• 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 61% compared to wild-type

abnormal leukocyte tethering or rolling ( J:48271 )

• Tnfa (TNFalpha) treatment increases leukocyte rolling flux fraction slightly compared to wild-type

• rolling velocities of leukocytes are slightly greater compared to wild-type mice at times <30 minutes after surgery; >60 minutes after surgery-induced inflammation, rolling velocities are significantly faster than wild-type (58 vs 38 um/second)

• similar results on rolling velocity are observed with Tnfa-activated rolling as induced by surgical trauma

homeostasis/metabolism

abnormal nitric oxide homeostasis ( J:118196 )

• in endothelial cell culture, Vegf-dependent and basal nitric oxide production is attenuated relative to wild-type cells

Genotype
MGI:3766730

hm2

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay
• Genetic Background: B6.129S7-Icam1^tm1Bay/J

mortality/aging

decreased susceptibility to parasitic infection induced morbidity/mortality ( J:193592 )

• only 2 of 6 mice infected with Plasmodium berghei succumb by day 6 compared with all wild-type C57BL/6 mice

• however, parasitemia is normal

premature death ( J:118466 )

• mutants and wild-type mice treated with streptozotocin to induce diabetes display significantly increased mortality after 12 months of disease compared to untreated controls

vision/eye

decreased susceptibility to induced choroidal neovascularization ( J:119416 )

• at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~75.7% compared to wild-type mice

• mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type

abnormal retina morphology ( J:118466 , J:119416 )

• in the galactose- and streptozotocin-induced diabetes models, after 11 months, mutants have fewer adherent leukocytes in the retina compared to diabetic controls; number of adherent leukocytes in the retina in 11-month diabetic mutants does not differ from number in non-diabetic controls (J:118466)

• diabetic wild-type mice at 11 months of disease have a 3.1-fold increase in adherent leukocyte number compared with non-diabetic controls (J:118466)

• compared to diabetic wild-type controls, number of endothelial cells in diabetic mutants are higher and comparable to non-diabetic wild-type controls (J:118466)

• 11-month diabetic wild-type mice have 3.8-fold more acellular capillaries compared to non-diabetic controls; in diabetic mutants, this pathology is suppressed by 56% with number of acellular capillaries similar to that in non-diabetic wild-type controls (J:118466)

• at 11 months, numbers of normal appearing pericytes in retinas of diabetic mutants are significantly greater than number in diabetic wild-type controls (J:118466)

• at 22 months, galactosemic mutants show almost less endothelial cell loss (19% vs 25% in galactosemic wild-type mice), no pericyte loss, and less acellular capillary formation (by 55%) than galactosemic wild-type controls compared to euglycemic wild-type mice (J:118466)

• no basement membrane thickening is observed in diabetic and galactosemic mutants compared to that observed in diabetic and galactosemic wild-type controls (J:118466)

• following laser photocoagulation (1,2, and 4 weeks after), significantly less pathologically significant leakage (fewer grade-2B lesions) develops in mutants compared to wild-type (J:119416)

• at weeks 1 and 4, mutants have fewer grade-2B lesions than wild-type mice (J:119416)

• mice have more nonleaky (grade 0) lesions than Icam1-null or wild-type mice at week 4 (J:119416)

abnormal retina vasculature morphology ( J:118466 )

• in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months

abnormal eye physiology ( J:118466 )

• in the diabetes models, 11-month diabetic mutants have decreased numbers of injured endothelial cells (<5%) compared to diabetic wild-type controls

cardiovascular system

decreased susceptibility to induced choroidal neovascularization ( J:119416 )

• at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~75.7% compared to wild-type mice

• mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type

abnormal retina vasculature morphology ( J:118466 )

• in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months

immune system

immune system phenotype ( J:193592 )

N • leukocytes exhibit normal adhesion in the brain of un-infected and Plasmodium berghei-infected mice

decreased susceptibility to parasitic infection induced morbidity/mortality ( J:193592 )

• only 2 of 6 mice infected with Plasmodium berghei succumb by day 6 compared with all wild-type C57BL/6 mice

• however, parasitemia is normal

homeostasis/metabolism

increased circulating glucose level ( J:118466 )

• blood glucose levels are significantly increased in mutants and controls with streptozotocin treatment or high galactose diet

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malaria		DOID:12365		J:193592

Genotype
MGI:3766601

hm3

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay
• Genetic Background: either: B6.129S7-Icam1^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)

hematopoietic system

abnormal leukocyte tethering or rolling ( J:31374 )

• blocking of L-selection with monoclonal antibodies reduces rolling flux fraction of leukocytes to ~30 from 49%, but causes a greater reduction to ~6% in wild-type

increased leukocyte cell number ( J:31374 )

• systemic leukocyte counts are ~7670/ul (~62% neutrophils, ~36% lymphocytes) compared to wild-type counts of ~5660/ul (53% neutrophils, 46% lymphocytes)

immune system

abnormal leukocyte tethering or rolling ( J:31374 )

• blocking of L-selection with monoclonal antibodies reduces rolling flux fraction of leukocytes to ~30 from 49%, but causes a greater reduction to ~6% in wild-type

increased leukocyte cell number ( J:31374 )

• systemic leukocyte counts are ~7670/ul (~62% neutrophils, ~36% lymphocytes) compared to wild-type counts of ~5660/ul (53% neutrophils, 46% lymphocytes)

cellular

abnormal leukocyte tethering or rolling ( J:31374 )

• blocking of L-selection with monoclonal antibodies reduces rolling flux fraction of leukocytes to ~30 from 49%, but causes a greater reduction to ~6% in wild-type

Genotype
MGI:3766946

hm4

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

immune system

decreased susceptibility to induced colitis ( J:111227 )

• DSS-treated mice show significantly attenuated colonic injury compared to DSS-treated wild-type mice; physical symptoms (disease activity index, diarrhea, rectal bleeding) and histopathological features (epithelial layer ulceration, sumbucosa edema, crypt damage) are reduced compared to wild-type controls

large intestinal inflammation ( J:111227 )

• mutants treated with dextran sodium sulfate (DSS) show attenuated eosinophilic inflammation and lower luminal erythropoietin activity than DSS-treated wild-type mice

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mutants and this increases with age of mice

impaired neutrophil recruitment ( J:112286 )

• dermal neutrophil emigration is reduced by 61% compared to wild-type in croton oil-induced dermatitis in 7-14 week old animals

hematopoietic system

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mutants and this increases with age of mice

impaired neutrophil recruitment ( J:112286 )

• dermal neutrophil emigration is reduced by 61% compared to wild-type in croton oil-induced dermatitis in 7-14 week old animals

digestive/alimentary system

decreased susceptibility to induced colitis ( J:111227 )

• DSS-treated mice show significantly attenuated colonic injury compared to DSS-treated wild-type mice; physical symptoms (disease activity index, diarrhea, rectal bleeding) and histopathological features (epithelial layer ulceration, sumbucosa edema, crypt damage) are reduced compared to wild-type controls

large intestinal inflammation ( J:111227 )

• mutants treated with dextran sodium sulfate (DSS) show attenuated eosinophilic inflammation and lower luminal erythropoietin activity than DSS-treated wild-type mice

Genotype
MGI:2179060

hm5

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

immune system

increased neutrophil cell number ( J:14565 )

• count in peripheral blood is increased to ~4.1x10⁵ in mutants from 1.0x10⁵ in controls at 2-4 months

• 3 hours after thioglycollate injection to induce peritonitis, neutrophil count in blood is elevated above resting state

abnormal immune system physiology ( J:14565 )

• spleen cells show a marked reduction in ability to function as stimulator cells in a mixed lymphocyte reaction (MLR) assay, compared to wild-type cells; however, isolated T cells respond similarly to wild-type cells to allogeneic stimulaton

abnormal cellular extravasation ( J:14565 )

• in an induced peritonitis model, total numbers of neutrophils that underwent transendothelial migration into the peritoneal cavity, as well as percentage of neutrophils relative to all leukocytes in exudate are reduced relative to controls

• 3 hours after thioglycollate injection to induce peritonitis, neutrophil count in blood is elevated above resting state and, 8 hours after peritonitis induction, peritonitis analysis shows 76% neutrophils wild-type compared to 43% in mutants; this indicates a defect in transendothelial migration, not just a delay

decreased susceptibility to type IV hypersensitivity reaction ( J:14565 )

• application of DTNB to the ear of mutant mice 7-19 weeks old 5 days following sensitization to DTNB shows a 74% reduction in ear swelling compared to wild-type after 24 hours

hematopoietic system

abnormal cellular extravasation ( J:14565 )

• in an induced peritonitis model, total numbers of neutrophils that underwent transendothelial migration into the peritoneal cavity, as well as percentage of neutrophils relative to all leukocytes in exudate are reduced relative to controls

• 3 hours after thioglycollate injection to induce peritonitis, neutrophil count in blood is elevated above resting state and, 8 hours after peritonitis induction, peritonitis analysis shows 76% neutrophils wild-type compared to 43% in mutants; this indicates a defect in transendothelial migration, not just a delay

increased neutrophil cell number ( J:14565 )

• count in peripheral blood is increased to ~4.1x10⁵ in mutants from 1.0x10⁵ in controls at 2-4 months

• 3 hours after thioglycollate injection to induce peritonitis, neutrophil count in blood is elevated above resting state

cellular

abnormal cellular extravasation ( J:14565 )

• in an induced peritonitis model, total numbers of neutrophils that underwent transendothelial migration into the peritoneal cavity, as well as percentage of neutrophils relative to all leukocytes in exudate are reduced relative to controls

• 3 hours after thioglycollate injection to induce peritonitis, neutrophil count in blood is elevated above resting state and, 8 hours after peritonitis induction, peritonitis analysis shows 76% neutrophils wild-type compared to 43% in mutants; this indicates a defect in transendothelial migration, not just a delay

Genotype
MGI:3766625

cx6

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Sell^tm1Tft/Sell^tm1Tft
• Genetic Background: B6.129-Sell^tm1Tft Icam1^tm1Bay

growth/size/body

increased body weight ( J:48271 )

• mice are ~20% heavier than wild-type or Sell^tm1Tft mutant mice

immune system

abnormal cellular extravasation ( J:48271 )

• 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 92% compared to wild-type

abnormal leukocyte tethering or rolling ( J:48271 )

• tumor necrosis factor alpha (Tnfa) treatment reduces leukocyte rolling flux below level seen in Sell^tm1Tft mutant mice

• rolling velocities of leukocytes are significantly greater at times <30 minutes after surgery compared to Sell^tm1Tft mutant mice (40 vs 19 um/second)

increased eosinophil cell number ( J:48271 )

• increased significantly compared to wild-type, comparable to Icam1-deficient mice

increased neutrophil cell number ( J:48271 )

• number of circulating neutrophils is increased over wild-type (580% of wild-type number)

increased lymphocyte cell number ( J:48271 )

• number of circulating lymphocytes is increased over wild-type (200% of wild-type number)

increased monocyte cell number ( J:48271 )

• number of circulating monocytes is increased over wild-type (640% of wild-type number)

abnormal mast cell physiology ( J:124291 )

• mast cell infiltration of tissue after wounding is lower in mutants with or without Sele/Selp blockade at 3 and 7 days compared to wild-type animals; bFGF or PDGF signifcantly increase mast cell infiltration at 3 and 7 days in mutants with Sele/Selp blockade

abnormal macrophage physiology ( J:124291 )

• macrophage infiltration is reduced at 3 and 7 days after wounding in mutants with or without Sele/Selp blockade relative to wild-type; numbers are reduced to greater degree with Sele/Selp blockade in mutants at 3 days but difference is not significant at 7 days

impaired macrophage chemotaxis ( J:124291 )

• numbers in tissue after wounding are lower in mutants compared to controls

• bFGF or PDGFsignifcantly increase macrophage infiltration at 3 and 7 days in mutants with Sele/Selp blockade

abnormal inflammatory response ( J:124291 )

• after wounding, levels of cytokine mRNAs including TNFalpha, Il6, Il10, and TGFbeta are all reduced in mutants with or without Sele/Selp blockade compared to controls

• bFGF or PDGF significantly increases CD3+ T cell infiltration at 3 and 7 days in mutants with Sele/Selp blockade

hematopoietic system

abnormal cellular extravasation ( J:48271 )

• 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 92% compared to wild-type

abnormal leukocyte tethering or rolling ( J:48271 )

• tumor necrosis factor alpha (Tnfa) treatment reduces leukocyte rolling flux below level seen in Sell^tm1Tft mutant mice

• rolling velocities of leukocytes are significantly greater at times <30 minutes after surgery compared to Sell^tm1Tft mutant mice (40 vs 19 um/second)

increased eosinophil cell number ( J:48271 )

• increased significantly compared to wild-type, comparable to Icam1-deficient mice

increased neutrophil cell number ( J:48271 )

• number of circulating neutrophils is increased over wild-type (580% of wild-type number)

increased lymphocyte cell number ( J:48271 )

• number of circulating lymphocytes is increased over wild-type (200% of wild-type number)

increased monocyte cell number ( J:48271 )

• number of circulating monocytes is increased over wild-type (640% of wild-type number)

abnormal mast cell physiology ( J:124291 )

• mast cell infiltration of tissue after wounding is lower in mutants with or without Sele/Selp blockade at 3 and 7 days compared to wild-type animals; bFGF or PDGF signifcantly increase mast cell infiltration at 3 and 7 days in mutants with Sele/Selp blockade

abnormal macrophage physiology ( J:124291 )

• macrophage infiltration is reduced at 3 and 7 days after wounding in mutants with or without Sele/Selp blockade relative to wild-type; numbers are reduced to greater degree with Sele/Selp blockade in mutants at 3 days but difference is not significant at 7 days

impaired macrophage chemotaxis ( J:124291 )

• numbers in tissue after wounding are lower in mutants compared to controls

• bFGF or PDGFsignifcantly increase macrophage infiltration at 3 and 7 days in mutants with Sele/Selp blockade

neoplasm

increased tumor growth/size ( J:108135 )

• when injected with melanoma cells, mice exhibit a 2.3 fold increase in tumor volume on day 7 compared to wild-type mice; difference in tumor volume is 5.8-fold compared to wild-type on day 14

cardiovascular system

decreased angiogenesis ( J:124291 )

• at 3 and 7 days following injury, vascular density in the wound bed in mutants with or without Sele and Selp blockade is less than that observed in wild-type controls; treatment with bFGF increases vascular vessel density at 3 days after wounding in mutants with Sele/Selp blockade, but this is not maintained at 7 days

homeostasis/metabolism

delayed wound healing ( J:124291 )

impaired wound healing ( J:124291 )

• excisional wound healing is impaired in mutant mice and mutants or wild-type mice with Sele and Selp inhibition by monoclonal antibodies compared to wild-type mice at 3 and 7 days after wounding

• open wound area at 3 and 7 days in mutants with or without antibody treatment is significantly larger than in untreated wild-type mice

• granulation tissue formation at 3 days after wounding is significantly less than controls; formation at 7 days is less than in wild-type with Sele and Selp blockade or mutants with Sele and Selp blockade; treatment of mutants with Sele/Selp blockade with bFGF and to a lesser extent with PDGF normalizes granulation tissue formation at 7 days after wounding

• addition of basic FGF (bFGF) significantly reduces open wound area at 7 days after wounding in mutants with Sele/Selp blockade

integument

decreased keratinocyte migration ( J:124291 )

• keratinocyte migration in wound healing is inhibited in mutants at 3 and 7 days compared to wild-type mice, and is further inhibited by Sele and Selp blockade; treatment with bFGF almost normalized keratinocyte migration in wounds by day 7 in mutants with Sele/Selp blockade

cellular

impaired macrophage chemotaxis ( J:124291 )

• numbers in tissue after wounding are lower in mutants compared to controls

• bFGF or PDGFsignifcantly increase macrophage infiltration at 3 and 7 days in mutants with Sele/Selp blockade

decreased keratinocyte migration ( J:124291 )

• keratinocyte migration in wound healing is inhibited in mutants at 3 and 7 days compared to wild-type mice, and is further inhibited by Sele and Selp blockade; treatment with bFGF almost normalized keratinocyte migration in wounds by day 7 in mutants with Sele/Selp blockade

abnormal cellular extravasation ( J:48271 )

• 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 92% compared to wild-type

abnormal leukocyte tethering or rolling ( J:48271 )

• tumor necrosis factor alpha (Tnfa) treatment reduces leukocyte rolling flux below level seen in Sell^tm1Tft mutant mice

• rolling velocities of leukocytes are significantly greater at times <30 minutes after surgery compared to Sell^tm1Tft mutant mice (40 vs 19 um/second)

Genotype
MGI:3767011

cx7

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: B6.129S7-Icam1^tm1Bay Selp^tm1Bay/J

nervous system

nervous system phenotype ( J:119906 )

N • no significant differences are detected in motor function (assessed at 1-5 days after CCI) or cognitive function (assessed at 14-20 days after injury) between mutants and wild-type mice

N • no significant differences are seen in contusion volume of the injured hemisphere or in volume of uninjured or injured hemisphere between wild-type and mutants 21 days after CCI

immune system

immune system phenotype ( J:119906 )

N • no difference in neutrophil accumulation at injury site at 24 hours after CCI is detected between mutant and wild-type mice

homeostasis/metabolism

edema ( J:119906 )

• brain edema at 24 hours after controlled cortical impact (CCI) is decreased in mutants compared to controls; brain water content ratio of injured and uninjured hemispheres) is lower (1.90) than in controls (3.16)

Genotype
MGI:3766607

cx8

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: either: B6.129S7-Selp^tm1Bay Icam1^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)

immune system

impaired leukocyte tethering or rolling ( J:31374 )

• double mutants show no spontaneous rolling leukocyte activity

• treatment with Tnfa induces leukocyte rolling although leukocytes show no spontaneous rolling activity; rolling flux fraction is ~22%, compared to ~36% in Icam1-deficient single mutants

cellular

impaired leukocyte tethering or rolling ( J:31374 )

• double mutants show no spontaneous rolling leukocyte activity

• treatment with Tnfa induces leukocyte rolling although leukocytes show no spontaneous rolling activity; rolling flux fraction is ~22%, compared to ~36% in Icam1-deficient single mutants

hematopoietic system

impaired leukocyte tethering or rolling ( J:31374 )

• double mutants show no spontaneous rolling leukocyte activity

• treatment with Tnfa induces leukocyte rolling although leukocytes show no spontaneous rolling activity; rolling flux fraction is ~22%, compared to ~36% in Icam1-deficient single mutants

Genotype
MGI:3766947

cx9

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Sele^tm2Alb/Sele^tm2Alb; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

immune system

impaired neutrophil chemotaxis ( J:112286 )

• migration is completely defective in acute croton oil dermatitis model in young mice (7-14 weeks); older mice show complete abrogation of neutrophil migration in response to irritation

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mice with acute croton oil dermatitis

decreased acute inflammation ( J:112286 )

• in response to croton oil application to the ear in young mice (7-14 weeks), inflammation is significantly reduced relative to controls

hematopoietic system

impaired neutrophil chemotaxis ( J:112286 )

• migration is completely defective in acute croton oil dermatitis model in young mice (7-14 weeks); older mice show complete abrogation of neutrophil migration in response to irritation

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mice with acute croton oil dermatitis

homeostasis/metabolism

skin edema ( J:112286 )

• dermal edema is decreased by 41% within 6 hours of croton oil irritation in young mice (7-14 weeks), and partial suppression of edema in older (23-35 weeks) mice

integument

integument phenotype ( J:112286 )

N • triply deficient mice do not develop spontaneous skin lesions up to 55 weeks of age

skin edema ( J:112286 )

• dermal edema is decreased by 41% within 6 hours of croton oil irritation in young mice (7-14 weeks), and partial suppression of edema in older (23-35 weeks) mice

cellular

impaired neutrophil chemotaxis ( J:112286 )

• migration is completely defective in acute croton oil dermatitis model in young mice (7-14 weeks); older mice show complete abrogation of neutrophil migration in response to irritation

Genotype
MGI:3606608

cx10

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

immune system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis eliminated neutrophil emigration into peritoneum

• Streptococcus pneumoniae induced pneumonia did not reduce neutrophil recruitment or edema formation in the alveolar space

increased neutrophil cell number ( J:24239 )

• 4-5 fold increase in numbers of circulating neutrophils

hematopoietic system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis eliminated neutrophil emigration into peritoneum

• Streptococcus pneumoniae induced pneumonia did not reduce neutrophil recruitment or edema formation in the alveolar space

increased neutrophil cell number ( J:24239 )

• 4-5 fold increase in numbers of circulating neutrophils

cellular

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis eliminated neutrophil emigration into peritoneum

• Streptococcus pneumoniae induced pneumonia did not reduce neutrophil recruitment or edema formation in the alveolar space