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Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Background Strain C57BL/6J Donor Strain 129S7 via AB1 ES cell line (+Hprt-bm2) Generation N6F5p Donating Investigator Arthur Beaudet, Baylor College of Medicine Appearance
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Related Genotype: a/aDescription
Mice homozygous for the Icam1tm1Bay targeted mutation are viable and fertile but lack surface ICAM1 expression. There is a mild increase in neutrophil count and impaired neutrophil emigration. Contact hypersensitivity is suppressed. A severe defect in T-cells does not allow function as stimulator cells in the mixed lymphocyte reaction. Mice from this targeted mutation express residual amounts of ICAM1 in the thymus and lung. ICAM1 expression is the result of alternative splicing of RNA causing the mutated exon 5 to be skipped causing three different alternative isoforms. Additional isoforms have been identified in wildtype mice. All alternatively spliced isoforms of ICAM1 detected are missing complete extracellular immunoglobulin domains. In addition, all, except one, retain the ability to bind to the counter-receptor LFA1.Development
The Icam1tm1Bay mutant strain was developed in the laboratory of Dr. Arthur Beaudet at Baylor College of Medicine. A targeting vector was used that resulted in the disruption of exon 5 of the Icam1 gene. The 129-derived AB1 ES cell line was used.
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Strains carrying Icam1tm1Bay allele
002285 B6.129S7-Icam1tm1Bay Selptm1Bay/J View Strains carrying Icam1tm1Bay (1 strain)
Strains carrying other alleles of Icam1
002867 B6.129S4-Icam1tm1Jcgr/J 006351 NOD.129S4(B6)-Icam1tm1Jcgr/J 005983 NOD.129S4(B6)-Icam1tm1Jcgr/SmtnJ View Strains carrying other alleles of Icam1 (3 strains)
Congenic Nomenclature
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
Icam1tm1Bay/Icam1tm1Bay
B6.129S7-Icam1tm1Bay
- growth/size phenotype
- increased body weight (MGI Ref ID J:48271)
- mice are ~20% heavier than wild-type or Selltm1Tft mutant mice
- immune system phenotype
- abnormal leukocyte migration/homing (MGI Ref ID J:24239)
- Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 64% after 4 hours
- abnormal leukocyte rolling (MGI Ref ID 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
- abnormal leukocyte transmigration (MGI Ref ID J:48271)
- 2 hours after thioglycollate-induced peritonitis, neutrophil entry into peritoneum is significantly inhibited by 61% compared to wild-type
- decreased susceptibility to endotoxin shock (MGI Ref ID 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
- increased eosinophil cell number (MGI Ref ID J:48271)
- increased significantly compared to wild-type (178% of wild-type)
- increased lymphocyte cell number (MGI Ref ID J:48271)
- number of circulating lymphocytes is increased over wild-type (47% of wild-type number)
- increased monocyte cell number (MGI Ref ID J:48271)
- number of circulating monocytes is increased over wild-type (223% of wild-type number)
- increased neutrophil cell number (MGI Ref ID J:24239)
- 4-5 fold increase in numbers of circulating neutrophils
- number of circulating neutrophils is increased over wild-type (190% of wild-type number)
- hematopoietic system phenotype
- increased eosinophil cell number (MGI Ref ID J:48271)
- increased significantly compared to wild-type (178% of wild-type)
- increased lymphocyte cell number (MGI Ref ID J:48271)
- number of circulating lymphocytes is increased over wild-type (47% of wild-type number)
- increased monocyte cell number (MGI Ref ID J:48271)
- number of circulating monocytes is increased over wild-type (223% of wild-type number)
- increased neutrophil cell number (MGI Ref ID J:24239)
- 4-5 fold increase in numbers of circulating neutrophils
- number of circulating neutrophils is increased over wild-type (190% of wild-type number)
- tumorigenesis
- increased tumor growth/size (MGI Ref ID 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
Icam1tm1Bay/Icam1tm1Bay
either: B6.129S7-Icam1tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)
- hematopoietic system phenotype
- increased leukocyte cell number (MGI Ref ID 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 phenotype
- abnormal leukocyte rolling (MGI Ref ID 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 (MGI Ref ID J:31374)
- systemic leukocyte counts are ~7670/ul (~62% neutrophils, ~36% lymphocytes) compared to wild-type counts of ~5660/ul (53% neutrophils, 46% lymphocytes)
Icam1tm1Bay/Icam1tm1Bay
B6.129S7-Icam1tm1Bay/J
- life span-post-weaning/aging
- premature death (MGI Ref ID 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 phenotype
- abnormal eye physiology (MGI Ref ID J:118466)
- in the diabetes models, 11-month diabetic mutants have decreased numbers of injured endothelial cells (<5%) compared to diabetic wild-type controls
- abnormal retina morphology (MGI Ref ID J:118466)
- 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
- diabetic wild-type mice at 11 months of disease have a 3.1-fold increase in adherent leukocyte number compared with non-diabetic controls
- compared to diabetic wild-type controls, number of endothelial cells in diabetic mutants are higher and comparable to non-diabetic wild-type controls
- 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
- at 11 months, numbers of normal appearing pericytes in retinas of diabetic mutants are significantly greater than number in diabetic wild-type controls
- 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
- no basement membrane thickening is observed in diabetic and galactosemic mutants compared to that observed in diabetic and galactosemic wild-type controls
- 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
- at weeks 1 and 4, mutants have fewer grade-2B lesions than wild-type mice
- mice have more nonleaky (grade 0) lesions than Icam1-null or wild-type mice at week 4
- abnormal retinal vasculature (MGI Ref ID J:118466)
- in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months
- increased resistance to induced choroidal neovascularization (MGI Ref ID 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
- homeostasis/metabolism phenotype
- increased circulating glucose level (MGI Ref ID J:118466)
- blood glucose levels are significantly increased in mutants and controls with streptozotocin treatment or high galactose diet
- cardiovascular system phenotype
- abnormal retinal vasculature (MGI Ref ID J:118466)
- in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months
- increased resistance to induced choroidal neovascularization (MGI Ref ID 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
Icam1tm1Bay/Icam1tm1Bay
B6.129S7-Icam1tm1Bay
- cardiovascular system phenotype
- decreased angiogenesis (MGI Ref ID 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 phenotype
- abnormal cell physiology (MGI Ref ID J:118196)
- endothelial cells show attenuated chemotactic response to Vegfa in transwell chemotactic assays compared with wild-type control cells
- abnormal cell migration (MGI Ref ID J:118196)
- homeostasis/metabolism phenotype
- abnormal nitric oxide homeostasis (MGI Ref ID J:118196)
- in endothelial cell culture, Vegf-dependent and basal nitric oxide production is attenuated relative to wild-type cells
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Icam1tm1Bay/Icam1tm1Bay
involves: 129S7/SvEvBrd * C57BL/6J
- immune system phenotype
- abnormal immune system physiology (MGI Ref ID 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 leukocyte transmigration (MGI Ref ID 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 (MGI Ref ID 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
- increased neutrophil cell number (MGI Ref ID 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
- hematopoietic system phenotype
- increased neutrophil cell number (MGI Ref ID 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
Icam1tm1Bay/Icam1tm1Bay
involves: 129S7/SvEvBrd * C57BL/6
- immune system phenotype
- impaired neutrophil recruitment (MGI Ref ID J:112286)
- dermal neutrophil emigration is reduced by 61% compared to wild-type in croton oil-induced dermatitis in 7-14 week old animals
- increased neutrophil cell number (MGI Ref ID J:112286)
- circulating neutrophils are increased in mutants and this increases with age of mice
- large intestinal inflammation (MGI Ref ID J:111227)
- mutants treated with dextran sodium sulfate (DSS) show attenuated eosinophilic inflammation and lower luminal erythropoietin activity than DSS-treated wild-type mice
- decreased susceptibility to induced colitis (MGI Ref ID 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
- hematopoietic system phenotype
- increased neutrophil cell number (MGI Ref ID J:112286)
- circulating neutrophils are increased in mutants and this increases with age of mice
- digestive/alimentary phenotype
- large intestinal inflammation (MGI Ref ID J:111227)
- mutants treated with dextran sodium sulfate (DSS) show attenuated eosinophilic inflammation and lower luminal erythropoietin activity than DSS-treated wild-type mice
- decreased susceptibility to induced colitis (MGI Ref ID 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
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Icam1tm1Bay relatedInternal/Organ Research
Wound Healing (delayed/impaired)
Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Immunodeficiency
Inflammation
| Allele Symbol | Icam1tm1Bay | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Baylor College of Medicine | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | CD54-; ICAM-1-; | ||
| Mutation Made By | Arthur Beaudet, Baylor College of Medicine | ||
| Strain of Origin | 129S7/SvEvBrd-Hprt1<+> | ||
| ES Cell Line Name | AB1 | ||
| ES Cell Line Strain | 129S7/SvEvBrd-Hprt1<+> | ||
| Gene Symbol and Name | Icam1, intercellular adhesion molecule 1 | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | BB2; CD54; ICAM; Icam-1; Ly-47; MALA-2; MGC:6195; P3.58; lymphocyte antigen 47; | ||
| Molecular Note | A neomycin resistance cassette was inserted into exon 5 of the gene. Subsequent analysis reported by King, et. al. (J:25530) revealed the presence of alternatively spliced transcripts in both wild-type and homozygous mutant mice. Protein expression was detected in mutant mice in medullary stromal cells of the thymus, as well as in the lung and spleen. Variable splicing of exons 2 through 6, encoding extracellular Ig domains, results in the production of 3 isoforms (2-6, 3-6, 4-6, where the numbers refer to spliced exons) in mutant mice. In addition to the 3 found in mutant mice, 2 other alternative splice forms including exon 5 were identified in wild-type mice. The reading frame and exons 1 and 7, encoding the signal sequence and both the transmembrane and cytosolic domains, are left intact in each isoform. [MGI Ref ID J:14565] [MGI Ref ID J:25530] | ||
Genotyping Protocols
Icam1tm1Bay, STD PCR, vers. 1
Helpful Links
Optimizing PCR Protocols
Sligh JE Jr; Ballantyne CM; Rich SS; Hawkins HK; Smith CW; Bradley A; Beaudet AL. 1993. Inflammatory and immune responses are impaired in mice deficient in intercellular adhesion molecule 1. Proc Natl Acad Sci U S A 90(18):8529-33. [PubMed: 8104338] [MGI Ref ID J:14565]
Bullard DC; Hurley LA; Lorenzo I; Sly LM; Beaudet AL; Staite ND. 1996. Reduced susceptibility to collagen-induced arthritis in mice deficient in intercellular adhesion molecule-1. J Immunol 157(7):3153-8. [PubMed: 8816427] [MGI Ref ID J:36071]
Hamaguchi Y; Nishizawa Y; Yasui M; Hasegawa M; Kaburagi Y; Komura K; Nagaoka T; Saito E; Shimada Y; Takehara K; Kadono T; Steeber DA; Tedder TF; Sato S. 2002. Intercellular adhesion molecule-1 and L-selectin regulate bleomycin-induced lung fibrosis. Am J Pathol 161(5):1607-18. [PubMed: 12414509] [MGI Ref ID J:79905]
Kadono T; Venturi GM; Steeber DA; Tedder TF. 2002. Leukocyte rolling velocities and migration are optimized by cooperative L-selectin and intercellular adhesion molecule-1 functions. J Immunol 169(8):4542-50. [PubMed: 12370391] [MGI Ref ID J:79530]
Kato A; Gabay C; Okaya T; Lentsch AB. 2002. Specific role of interleukin-1 in hepatic neutrophil recruitment after ischemia/reperfusion. Am J Pathol 161(5):1797-803. [PubMed: 12414526] [MGI Ref ID J:79907]
King PD; Sandberg ET; Selvakumar A; Fang P; Beaudet AL; Dupont B. 1995. Novel isoforms of murine intercellular adhesion molecule-1 generated by alternative RNA splicing. J Immunol 154(11):6080-6093. [PubMed: 7751650] [MGI Ref ID J:25530]
Lacha J; Bushell A; Smetana K; Rossmann P; Pribylova P; Wood K; Maly P. 2002. Intercellular cell adhesion molecule-1 and selectin ligands in acute cardiac allograft rejection: a study on gene-deficient mouse models. J Leukoc Biol 71(2):311-8. [PubMed: 11818453] [MGI Ref ID J:74694]
Murray HW; Lu CM; Brooks EB; Fichtl RE; DeVecchio JL; Heinzel FP. 2003. Modulation of T-cell costimulation as immunotherapy or immunochemotherapy in experimental visceral leishmaniasis. Infect Immun 71(11):6453-62. [PubMed: 14573667] [MGI Ref ID J:86275]
Nagaoka T; Kaburagi Y; Hamaguchi Y; Hasegawa M; Takehara K; Steeber DA; Tedder TF; Sato S. 2000. Delayed wound healing in the absence of intercellular adhesion molecule-1 or L-selectin expression. Am J Pathol 157(1):237-47. [PubMed: 10880393] [MGI Ref ID J:63135]
Selzner N; Selzner M; Odermatt B; Tian Y; Van Rooijen N; Clavien PA. 2003. ICAM-1 triggers liver regeneration through leukocyte recruitment and Kupffer cell-dependent release of TNF-alpha/IL-6 in mice. Gastroenterology 124(3):692-700. [PubMed: 12612908] [MGI Ref ID J:82107]
Shimizu A; Sasaki H; Aoyagi K; Yoshida M; Kato K; Heike Y; Ikarashi Y; Shirakawa K; Takaue Y; Miyajima A; Terada M; Nagai H; Wakasugi H. 2004. The mouse natural killer T cell-associated antigen recognized by U5A2-13 monoclonal antibody is intercellular adhesion molecule-1. Immunol Lett 92(3):227-35. [PubMed: 15081617] [MGI Ref ID J:89516]
Sun G; Chang WL; Li J; Berney SM; Kimpel D; van der Heyde HC. 2003. Inhibition of platelet adherence to brain microvasculature protects against severe Plasmodium berghei malaria. Infect Immun 71(11):6553-61. [PubMed: 14573677] [MGI Ref ID J:86276]
Icam1tm1Bay relatedAoudjit F; Potworowski EF; Springer TA; St-Pierre Y. 1998. Protection from lymphoma cell metastasis in ICAM-1 mutant mice: a posthoming event. J Immunol 161(5):2333-8. [PubMed: 9725228] [MGI Ref ID J:49717]
Avellino AM; Dailey AT; Harlan JM; Sharar SR; Winn RK; McNutt LD; Kliot M. 2004. Blocking of up-regulated ICAM-1 does not prevent macrophage infiltration during Wallerian degeneration of peripheral nerve. Exp Neurol 187(2):430-44. [PubMed: 15144869] [MGI Ref ID J:90583]
Baker PJ; DuFour L; Dixon M; Roopenian DC. 2000. Adhesion molecule deficiencies increase Porphyromonas gingivalis-induced alveolar bone loss in mice. Infect Immun 68(6):3103-7. [PubMed: 10816450] [MGI Ref ID J:62266]
Bendjelloul F; Maly P; Mandys V; Jirkovska M; Prokesova L; Tuckova L; Tlaskalova-Hogenova H. 2000. Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis. Clin Exp Immunol 119(1):57-63. [PubMed: 10606964] [MGI Ref ID J:110249]
Berberich S; Dahne S; Schippers A; Peters T; Muller W; Kremmer E; Forster R; Pabst O. 2008. Differential molecular and anatomical basis for B cell migration into the peritoneal cavity and omental milky spots. J Immunol 180(4):2196-203. [PubMed: 18250426] [MGI Ref ID J:132002]
Bourdillon MC; Poston RN; Covacho C; Chignier E; Bricca G; McGregor JL. 2000. ICAM-1 deficiency reduces atherosclerotic lesions in double-knockout mice (ApoE(-/-)/ICAM-1(-/-)) fed a fat or a chow diet. Arterioscler Thromb Vasc Biol 20(12):2630-5. [PubMed: 11116064] [MGI Ref ID J:103384]
Briaud SA; Ding ZM; Michael LH; Entman ML; Daniel S; Ballantyne CM. 2001. Leukocyte trafficking and myocardial reperfusion injury in ICAM-1/P-selectin-knockout mice. Am J Physiol Heart Circ Physiol 280(1):H60-7. [PubMed: 11123218] [MGI Ref ID J:68056]
Broide DH; Humber D; Sullivan S; Sriramarao P. 1998. Inhibition of eosinophil rolling and recruitment in P-selectin- and intracellular adhesion molecule-1-deficient mice [published erratum appears in Blood 1998 Jul 1;92(1):343] Blood 91(8):2847-56. [PubMed: 9531595] [MGI Ref ID J:47461]
Broide DH; Sullivan S; Gifford T; Sriramarao P. 1998. Inhibition of pulmonary eosinophilia in P-selectin- and ICAM-1-deficient mice. Am J Respir Cell Mol Biol 18(2):218-25. [PubMed: 9476909] [MGI Ref ID J:114264]
Bullard DC; Hurley LA; Lorenzo I; Sly LM; Beaudet AL; Staite ND. 1996. Reduced susceptibility to collagen-induced arthritis in mice deficient in intercellular adhesion molecule-1. J Immunol 157(7):3153-8. [PubMed: 8816427] [MGI Ref ID J:36071]
Bullard DC; King PD; Hicks MJ; Dupont B; Beaudet AL; Elkon KB. 1997. Intercellular adhesion molecule-1 deficiency protects MRL/MpJ-Fas(lpr) mice from early lethality. J Immunol 159(4):2058-67. [PubMed: 9257874] [MGI Ref ID J:42669]
Bullard DC; Qin L; Lorenzo I; Quinlin WM; Doyle NA; Bosse R; Vestweber D; Doerschuk CM; Beaudet AL. 1995. P-selectin/ICAM-1 double mutant mice: acute emigration of neutrophils into the peritoneum is completely absent but is normal into pulmonary alveoli [see comments] J Clin Invest 95(4):1782-8. [PubMed: 7535798] [MGI Ref ID J:24239]
Calingasan NY; Huang PL; Chun HS; Fabian A; Gibson GE. 2000. Vascular factors are critical in selective neuronal loss in an animal model of impaired oxidative metabolism. J Neuropathol Exp Neurol 59(3):207-17. [PubMed: 10744059] [MGI Ref ID J:62409]
Carrithers MD; Visintin I; Viret C; Janeway CS Jr. 2002. Role of genetic background in P selectin-dependent immune surveillance of the central nervous system. J Neuroimmunol 129(1-2):51-7. [PubMed: 12161020] [MGI Ref ID J:102957]
Collins RG; Velji R; Guevara NV; Hicks MJ; Chan L; Beaudet AL. 2000. P-Selectin or intercellular adhesion molecule (ICAM)-1 deficiency substantially protects against atherosclerosis in apolipoprotein E-deficient mice. J Exp Med 191(1):189-94. [PubMed: 10620617] [MGI Ref ID J:59249]
Dautigny N; Le Campion A; Lucas B. 1999. Timing and casting for actors of thymic negative selection. J Immunol 162(3):1294-302. [PubMed: 9973382] [MGI Ref ID J:124433]
Davis SL; Hawkins EP; Mason EO Jr; Smith CW; Kaplan SL. 1996. Host defenses against disseminated candidiasis are impaired in intercellular adhesion molecule 1-deficient mice. J Infect Dis 174(2):435-9. [PubMed: 8699084] [MGI Ref ID J:34394]
Doerschuk CM; Quinlan WM; Doyle NA; Bullard DC; Vestweber D; Jones ML; Takei F; Ward PA; Beaudet AL. 1996. The role of P-selectin and ICAM-1 in acute lung injury as determined using blocking antibodies and mutant mice. J Immunol 157(10):4609-14. [PubMed: 8906840] [MGI Ref ID J:37197]
Emoto M; Emoto Y; Brinkmann V; Miyamoto M; Yoshizawa I; Staber M; van Rooijen N; Hamann A; Kaufmann SH. 2003. Increased resistance of LFA-1-deficient mice to lipopolysaccharide-induced shock/liver injury in the presence of TNF-alpha and IL-12 is mediated by IL-10: a novel role for LFA-1 in the regulation of the proinflammatory and anti-inflammatory cytokine balance. J Immunol 171(2):584-93. [PubMed: 12847222] [MGI Ref ID J:123460]
Emoto M; Mittrucker HW; Schmits R; Mak TW; Kaufmann SH. 1999. Critical role of leukocyte function-associated antigen-1 in liver accumulation of CD4+NKT cells. J Immunol 162(9):5094-8. [PubMed: 10227978] [MGI Ref ID J:111009]
Eppihimer MJ; Russell J; Anderson DC; Wolitzky BA; Granger DN. 1997. Endothelial cell adhesion molecule expression in gene-targeted mice. Am J Physiol 273(4 Pt 2):H1903-8. [PubMed: 9362259] [MGI Ref ID J:43907]
Fogler WE; Volker K; Watanabe M; Wigginton JM; Roessler P; Brunda MJ; Ortaldo JR; Wiltrout RH. 1998. Recruitment of hepatic NK cells by IL-12 is dependent on IFN-gamma and VCAM-1 and is rapidly down-regulated by a mechanism involving T cells and expression of Fas. J Immunol 161(11):6014-21. [PubMed: 9834083] [MGI Ref ID J:115033]
Forbes E; Hulett M; Ahrens R; Wagner N; Smart V; Matthaei KI; Brandt EB; Dent LA; Rothenberg ME; Tang M; Foster PS; Hogan SP. 2006. ICAM-1-dependent pathways regulate colonic eosinophilic inflammation. J Leukoc Biol 80(2):330-41. [PubMed: 16731772] [MGI Ref ID J:111227]
Furusho S; Myou S; Fujimura M; Kita T; Yasui M; Kasahara K; Nakao S; Takehara K; Sato S. 2006. Role of intercellular adhesion molecule-1 in a murine model of toluene diisocyanate-induced asthma. Clin Exp Allergy 36(10):1294-302. [PubMed: 17014439] [MGI Ref ID J:135960]
Graciano AL; Bryant DD; White DJ; Horton J; Bowles NE; Giroir BP. 2001. Targeted disruption of ICAM-1, P-selectin genes improves cardiac function and survival in TNF-alpha transgenic mice. Am J Physiol Heart Circ Physiol 280(4):H1464-71. [PubMed: 11247755] [MGI Ref ID J:108278]
Gregoire FM; Zhang Q; Smith SJ; Tong C; Ross D; Lopez H; West DB. 2002. Diet-induced obesity and hepatic gene expression alterations in C57BL/6J and ICAM-1-deficient mice. Am J Physiol Endocrinol Metab 282(3):E703-13. [PubMed: 11832376] [MGI Ref ID J:75612]
Gurish MF; Tao H; Abonia JP; Arya A; Friend DS; Parker CM; Austen KF. 2001. Intestinal mast cell progenitors require CD49dbeta7 (alpha4beta7 integrin) for tissue-specific homing. J Exp Med 194(9):1243-52. [PubMed: 11696590] [MGI Ref ID J:119138]
Hafezi-Moghadam A; Thomas KL; Prorock AJ; Huo Y; Ley K. 2001. L-selectin shedding regulates leukocyte recruitment. J Exp Med 193(7):863-72. [PubMed: 11283159] [MGI Ref ID J:120579]
Hallahan DE; Virudachalam S. 1997. Intercellular adhesion molecule 1 knockout abrogates radiation induced pulmonary inflammation. Proc Natl Acad Sci U S A 94(12):6432-7. [PubMed: 9177235] [MGI Ref ID J:111185]
Hamaguchi Y; Nishizawa Y; Yasui M; Hasegawa M; Kaburagi Y; Komura K; Nagaoka T; Saito E; Shimada Y; Takehara K; Kadono T; Steeber DA; Tedder TF; Sato S. 2002. Intercellular adhesion molecule-1 and L-selectin regulate bleomycin-induced lung fibrosis. Am J Pathol 161(5):1607-18. [PubMed: 12414509] [MGI Ref ID J:79905]
Hancock WW; Tsai TL; Madaio MP; Gasser DL. 2003. Cutting Edge: Multiple autoimmune pathways in kd/kd mice. J Immunol 171(6):2778-81. [PubMed: 12960297] [MGI Ref ID J:85380]
Hoefer IE; van Royen N; Rectenwald JE; Deindl E; Hua J; Jost M; Grundmann S; Voskuil M; Ozaki CK; Piek JJ; Buschmann IR. 2004. Arteriogenesis proceeds via ICAM-1/Mac-1- mediated mechanisms. Circ Res 94(9):1179-85. [PubMed: 15059933] [MGI Ref ID J:98899]
Horie Y; Wolf R; Anderson DC; Granger DN. 1997. Hepatic leukostasis and hypoxic stress in adhesion molecule-deficient mice after gut ischemia/reperfusion. J Clin Invest 99(4):781-8. [PubMed: 9045883] [MGI Ref ID J:39161]
Huleatt JW; Lefrancois L. 1996. Beta2 integrins and ICAM-1 are involved in establishment of the intestinal mucosal T cell compartment. Immunity 5(3):263-73. [PubMed: 8808681] [MGI Ref ID J:35355]
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Diet Information LabDiet® 5K52/5K67
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| 000664 C57BL/6J | ||
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