Strain Name:

B6.129S7-Itgb2tm1Bay/J

Stock Number:

002128

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Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. This strain serves as a model for the moderate form of human CD18 deficiency.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain 129S7 via AB1 ES cell line (+Hprt-bm2)
GenerationN10F45 (12-NOV-08)
Generation Definitions
 
Donating InvestigatorDr. Arthur Beaudet,   Baylor College of Medicine

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Itgb2tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency.

Development
The Itgb2tm1Bay mutant strain was developed in the laboratory of Dr. Arthur Beaudet at Baylor College of Medicine. The 129-derived AB1 ES cell line was used. The C57BL/6J strain was produced by backcrossing the Itgb2tm1Bay mutation 10 times to C57BL/6J inbred mice.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Itgb2
018648   B6.129S6(Cg)-Itgb2tm1.1Mskim/J
003329   B6.129S7-Itgb2tm2Bay/J
016897   NOD.129S7(B6)-Itgb2tm2Bay/CgkJ
View Strains carrying other alleles of Itgb2     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Leukocyte Adhesion Deficiency, Type I; LAD
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Itgb2tm1Bay/Itgb2tm1Bay

        B6.129S7-Itgb2tm1Bay/J
  • mortality/aging
  • premature death
    • mutants and wild-type mice treated with streptozotocin to induce diabetes display significantly increased mortality after 12 months of disease compared to untreated controls   (MGI Ref ID J:118466)
  • vision/eye phenotype
  • abnormal eye physiology
    • in the diabetes models, 11-month diabetic mutants have decreased numbers of injured endothelial cells (<5%) compared to diabetic wild-type controls   (MGI Ref ID J:118466)
  • abnormal retina morphology
    • 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   (MGI Ref ID 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   (MGI Ref ID 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   (MGI Ref ID 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 60% with number of acellular capillaries similar to that in non-diabetic wild-type controls   (MGI Ref ID 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   (MGI Ref ID J:118466)
    • at 22 months, galactosemic mutants show almost no endothelial cell loss, no pericyte loss, and less acellular capillary formation (by 60%) than galactosemic wild-type controls compared to euglycemic wild-type mice   (MGI Ref ID J:118466)
    • no basement membrane thickening is observed in diabetic and galactosemic mutants compared to that observed in diabetic and galactosemic wild-type controls   (MGI Ref ID 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   (MGI Ref ID J:119416)
    • less mice have 3 or more grade-2B lesions in each eye compared with wild-type   (MGI Ref ID J:119416)
    • abnormal retinal vasculature morphology
      • in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months   (MGI Ref ID J:118466)
  • decreased susceptibility to induced choroidal neovascularization
    • at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~67.0% compared to wild-type mice   (MGI Ref ID J:119416)
    • mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type   (MGI Ref ID J:119416)
  • homeostasis/metabolism phenotype
  • increased circulating glucose level
    • blood glucose levels are significantly increased in mutants and controls with streptozotocin treatment or high galactose diet   (MGI Ref ID J:118466)
  • cardiovascular system phenotype
  • abnormal retinal vasculature morphology
    • in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months   (MGI Ref ID J:118466)
  • decreased susceptibility to induced choroidal neovascularization
    • at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~67.0% compared to wild-type mice   (MGI Ref ID J:119416)
    • mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type   (MGI Ref ID J:119416)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Itgb2tm1Bay/Itgb2tm1Bay

        involves: 129S7/SvEvBrd
  • immune system phenotype
  • decreased inflammatory response
    • decreased inflammatory response to i.p. injection of thioglycollate showing decreased migration of neutrophils into the peritoneal cavity   (MGI Ref ID J:13599)
    • delayed rejection of cardiac transplants   (MGI Ref ID J:13599)
  • increased leukocyte cell number   (MGI Ref ID J:13599)
    • increased total leukocyte counts however less elevated than on the PL/J background   (MGI Ref ID J:32126)
    • increased granulocyte number   (MGI Ref ID J:13599)
    • increased lymphocyte cell number   (MGI Ref ID J:13599)
  • hematopoietic system phenotype
  • increased leukocyte cell number   (MGI Ref ID J:13599)
    • increased total leukocyte counts however less elevated than on the PL/J background   (MGI Ref ID J:32126)
    • increased granulocyte number   (MGI Ref ID J:13599)
    • increased lymphocyte cell number   (MGI Ref ID J:13599)
  • integument phenotype
  • *normal* integument phenotype
    • did not develop progressive dermatitis in the 129S7/SvEvBrd background   (MGI Ref ID J:32126)

Itgb2tm1Bay/Itgb2tm1Bay

        involves: 129S7/SvEvBrd * PL/J
  • immune system phenotype
  • abnormal T cell activation
    • mice show increased state of activation in CD4+ T cells   (MGI Ref ID J:109598)
  • abnormal cytokine level
    • increase in Th1 cytokines, IFN-gamma, IL-2, and IL-10, in T cells from skin lesion-draining lymph nodes   (MGI Ref ID J:109598)
  • abnormal spleen morphology
    • exhibited myeloid hyperplasia in the spleen   (MGI Ref ID J:32126)
  • dermatitis
    • developed a progressive dermatitis, characterized by erythema, alopecia, and scale and crust formation   (MGI Ref ID J:32126)
    • mice develop psoriasiform dermatitis   (MGI Ref ID J:109598)
    • depletion of CD4+ T cells, but not of CD8+ T cells, with depleting antibodies results in resolution of the psoriasiform dermatitis after 6 weeks of treatment   (MGI Ref ID J:109598)
  • enlarged lymph nodes
    • displayed reactive lymphadenopathy   (MGI Ref ID J:32126)
  • increased interferon-gamma secretion
    • CD90+ T cells release up to 40-fold higher concentrations of IFN-gamma when cultured with anti-CD3 and anti-CD28 antibodies   (MGI Ref ID J:109598)
  • increased leukocyte cell number
    • numbers of white blood cells were increased to a higher extent than on a 129S7/SvEvBrd background   (MGI Ref ID J:32126)
    • increased basophil cell number   (MGI Ref ID J:32126)
    • increased eosinophil cell number   (MGI Ref ID J:32126)
    • increased lymphocyte cell number   (MGI Ref ID J:32126)
      • increased T cell number
        • number of CD4+ and CD8+ T cells is highly increased in the epidermis and dermis   (MGI Ref ID J:109598)
        • increased T-helper 1 cell number
          • increase in Th1-type cytokine-producing CD4+ T cells but not in Th2-type cytokine producing T cells   (MGI Ref ID J:109598)
    • increased monocyte cell number   (MGI Ref ID J:32126)
    • increased neutrophil cell number   (MGI Ref ID J:32126)
  • myeloid hyperplasia
    • exhibited myeloid hyperplasia in the bone marrow   (MGI Ref ID J:32126)
  • hematopoietic system phenotype
  • abnormal T cell activation
    • mice show increased state of activation in CD4+ T cells   (MGI Ref ID J:109598)
  • abnormal spleen morphology
    • exhibited myeloid hyperplasia in the spleen   (MGI Ref ID J:32126)
  • increased leukocyte cell number
    • numbers of white blood cells were increased to a higher extent than on a 129S7/SvEvBrd background   (MGI Ref ID J:32126)
    • increased basophil cell number   (MGI Ref ID J:32126)
    • increased eosinophil cell number   (MGI Ref ID J:32126)
    • increased lymphocyte cell number   (MGI Ref ID J:32126)
      • increased T cell number
        • number of CD4+ and CD8+ T cells is highly increased in the epidermis and dermis   (MGI Ref ID J:109598)
        • increased T-helper 1 cell number
          • increase in Th1-type cytokine-producing CD4+ T cells but not in Th2-type cytokine producing T cells   (MGI Ref ID J:109598)
    • increased monocyte cell number   (MGI Ref ID J:32126)
    • increased neutrophil cell number   (MGI Ref ID J:32126)
  • increased platelet cell number   (MGI Ref ID J:32126)
  • myeloid hyperplasia
    • exhibited myeloid hyperplasia in the bone marrow   (MGI Ref ID J:32126)
  • pigmentation phenotype
  • *normal* pigmentation phenotype
    • associated phenotype appears on the PL/J background but not on a C57BL/6 or 129S7/SvEvBrd background   (MGI Ref ID J:32126)
  • integument phenotype
  • *normal* integument phenotype
    • associated phenotypes appear on the PL/J background but not on a C57BL/6 or 129S7/SvEvBrd background   (MGI Ref ID J:32126)
    • abnormal dermal layer morphology
      • dermal collagen appeared disorganized   (MGI Ref ID J:32126)
      • mixed cellular infiltration to dermis
        • progressive dermatitis with a dermal infiltrate consisting of granulocytes, lymphocytes, histiocytes and scattered mast cells   (MGI Ref ID J:32126)
    • abnormal epidermal layer morphology
      • occasionally developed focal spongiosis and erosion of the epidermis   (MGI Ref ID J:32126)
      • epidermal hyperplasia
        • irregular psoriasiform hyperplasia of the epidermis   (MGI Ref ID J:32126)
      • orthokeratosis
        • skin exhibited orthohyperkeratosis   (MGI Ref ID J:32126)
      • parakeratosis   (MGI Ref ID J:32126)
    • abnormal hair follicle dermal papilla morphology
      • vessels within the dermal papillae were dilated   (MGI Ref ID J:32126)
    • abnormal skin condition   (MGI Ref ID J:32126)
      • psoriasis
        • had irregular psoriasiform hyperplasia of the epidermis and subcorneal microabscesses   (MGI Ref ID J:32126)
        • mice develop psoriasiform dermatitis   (MGI Ref ID J:109598)
    • alopecia   (MGI Ref ID J:109598)
      • progressively developed in the facial region and/or base of the tail   (MGI Ref ID J:32126)
    • dermatitis
      • developed a progressive dermatitis, characterized by erythema, alopecia, and scale and crust formation   (MGI Ref ID J:32126)
      • mice develop psoriasiform dermatitis   (MGI Ref ID J:109598)
      • depletion of CD4+ T cells, but not of CD8+ T cells, with depleting antibodies results in resolution of the psoriasiform dermatitis after 6 weeks of treatment   (MGI Ref ID J:109598)
    • reddish skin
      • dermatitis was characterized by erythema   (MGI Ref ID J:32126)
    • scaly skin   (MGI Ref ID J:109598)
      • severely affected mice developed scales and crusts in the dorsum of the trunk, the abdomen, and the neck   (MGI Ref ID J:32126)
  • homeostasis/metabolism phenotype
  • abnormal cytokine level
    • increase in Th1 cytokines, IFN-gamma, IL-2, and IL-10, in T cells from skin lesion-draining lymph nodes   (MGI Ref ID J:109598)

Itgb2tm1Bay/Itgb2tm1Bay

        involves: 129S7/SvEvBrd * C57BL/6J
  • immune system phenotype
  • abnormal spleen red pulp morphology
    • myeloid hyperplasia of splenic red pulp   (MGI Ref ID J:13599)
  • myeloid hyperplasia
    • myeloid hyperplasia in bone marrow   (MGI Ref ID J:13599)
  • hematopoietic system phenotype
  • abnormal spleen red pulp morphology
    • myeloid hyperplasia of splenic red pulp   (MGI Ref ID J:13599)
  • myeloid hyperplasia
    • myeloid hyperplasia in bone marrow   (MGI Ref ID J:13599)
  • integument phenotype
  • *normal* integument phenotype
    • did not develop progressive dermatitis in the C57BL/6J background   (MGI Ref ID J:32126)

Itgb2tm1Bay/Itgb2tm1Bay

        involves: 129S7/SvEvBrd * C57BL/6J * PL/J
  • immune system phenotype
  • dermatitis
    • 23.5% of the F2 progeny from a PL/J x C57BL/6J intercross develop psoriasiform dermatitis, which is not observed on a 129S7/SvEvBrd or a mixed 129S7/SvEvBrd and C57BL/6J background   (MGI Ref ID J:84126)
  • integument phenotype
  • *normal* integument phenotype   (MGI Ref ID J:84126)
    • F1 mice from intercrosses of homozygotes on PL/J and C57BL/6J backgrounds did not develop progressive dermatitis, however when F1 mice were backcrossed to homozygotes on the PL/J background, 50% developed dermatitis   (MGI Ref ID J:32126)
    • alopecia
      • approximately half of affected F2 mice develop severe disease with various degrees of alopecia   (MGI Ref ID J:84126)
    • dermatitis
      • 23.5% of the F2 progeny from a PL/J x C57BL/6J intercross develop psoriasiform dermatitis, which is not observed on a 129S7/SvEvBrd or a mixed 129S7/SvEvBrd and C57BL/6J background   (MGI Ref ID J:84126)
    • psoriasis
      • 23.5% of the F2 progeny from a PL/J x C57BL/6J intercross develop chronic inflammatory skin disease with highly variable severity   (MGI Ref ID J:84126)
    • reddish skin
      • approximately half of affected F2 mice develop only mild disease with erythema and/or dry skin, which is not observed on a 129S7/SvEvBrd or a mixed 129S7/SvEvBrd and C57BL/6J background   (MGI Ref ID J:84126)
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Research Applications
This mouse can be used to support research in many areas including:

Itgb2tm1Bay related

Cell Biology Research
Defects in Cell Adhesion Molecules

Dermatology Research
Skin and Hair Texture Defects

Developmental Biology Research
Defects in Cell Adhesion Molecules
Defects in Extracellular Matrix Molecules

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Inflammation

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Itgb2tm1Bay
Allele Name targeted mutation 1, Baylor College of Medicine
Allele Type Targeted (Hypomorph)
Common Name(s) CD18-; CD18hypo; CD18low; Itgb2hypo;
Mutation Made ByDr. Arthur Beaudet,   Baylor College of Medicine
Strain of Origin129S7/SvEvBrd-Hprt<+>
ES Cell Line NameAB1
ES Cell Line Strain129S7/SvEvBrd-Hprt<+>
Gene Symbol and Name Itgb2, integrin beta 2
Chromosome 10
Gene Common Name(s) 2E6; AI528527; CD18; CD18 antigen; Cd18; LAD; LCAMB; LFA-1; MAC-1; MF17; MFI7; Mac-1 beta; expressed sequence AI528527;
General Note Homozygous or trans heterozgous mice (Itgb2tm1Bay / Itgb2tm2Bay) on a mixed background that includes the strain PL/J and trans heterozygous mice on a congenic PL/J background display Phenotypic Similarity to Human Syndrome: Psoriasis. However, mice on backgrounds that do not include PL/J do not display psoriasis. (J:32126, J:84126, J:109598, J:207148)
Molecular Note An insertion mutation that duplicates exons 2 and 3 with interruption of one copy of exon 3 with a neomycin cassette. This is not a null mutation but rather a hypomorph expressing very low levels of ITGB2 protein. [MGI Ref ID J:13599]

Genotyping

Genotyping Information

Genotyping Protocols

Itgb2tm1Bay, QPCR
Itgb2tm1Bay, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Wilson RW; Ballantyne CM; Smith CW; Montgomery C; Bradley A; O'Brien WE; Beaudet AL. 1993. Gene targeting yields a CD18-mutant mouse for study of inflammation. J Immunol 151(3):1571-8. [PubMed: 8101543]  [MGI Ref ID J:13599]

Additional References

Bullard DC; Scharffetter-Kochanek K; McArthur MJ; Chosay JG; McBride ME; Montgomery CA; Beaudet AL. 1996. A polygenic mouse model of psoriasiform skin disease in CD18-deficient mice. Proc Natl Acad Sci U S A 93(5):2116-21. [PubMed: 8700894]  [MGI Ref ID J:32126]

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]

Papayannopoulou T; Priestley GV; Nakamoto B; Zafiropoulos V; Scott LM; Harlan JM. 2001. Synergistic mobilization of hemopoietic progenitor cells using concurrent beta1 and beta2 integrin blockade or beta2-deficient mice. Blood 97(5):1282-8. [PubMed: 11222371]  [MGI Ref ID J:67767]

Wu HS; Kolonoski P; Chang YY; Bermudez LE. 2000. Invasion of the brain and chronic central nervous system infection after systemic Mycobacterium avium complex infection in mice. Infect Immun 68(5):2979-84. [PubMed: 10768998]  [MGI Ref ID J:61694]

Itgb2tm1Bay related

Ahn GO; Tseng D; Liao CH; Dorie MJ; Czechowicz A; Brown JM. 2010. Inhibition of Mac-1 (CD11b/CD18) enhances tumor response to radiation by reducing myeloid cell recruitment. Proc Natl Acad Sci U S A 107(18):8363-8. [PubMed: 20404138]  [MGI Ref ID J:160334]

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]

Barlow SC; Collins RG; Ball NJ; Weaver CT; Schoeb TR; Bullard DC. 2003. Psoriasiform Dermatitis Susceptibility in Itgb2(tm1Bay) PL/J Mice Requires Low-Level CD18 Expression and at Least Two Additional Loci for Progression to Severe Disease. Am J Pathol 163(1):197-202. [PubMed: 12819024]  [MGI Ref ID J:84126]

Barlow SC; Xu H; Weaver CT; Lindsey JR; Schoeb TR; Bullard DC. 2004. Development of dermatitis in CD18-deficient PL/J mice is not dependent on bacterial flora, and requires both CD4+ and CD8+ T lymphocytes. Int Immunol 16(2):345-51. [PubMed: 14734620]  [MGI Ref ID J:88930]

Bullard DC; Scharffetter-Kochanek K; McArthur MJ; Chosay JG; McBride ME; Montgomery CA; Beaudet AL. 1996. A polygenic mouse model of psoriasiform skin disease in CD18-deficient mice. Proc Natl Acad Sci U S A 93(5):2116-21. [PubMed: 8700894]  [MGI Ref ID J:32126]

Daley JM; Ivanenko-Johnston T; Reichner JS; Albina JE. 2005. Transcriptional regulation of TNF-alpha production in neutropenia. Am J Physiol Regul Integr Comp Physiol 288(2):R409-12. [PubMed: 15458967]  [MGI Ref ID J:104758]

Dearth CL; Goh Q; Marino JS; Cicinelli PA; Torres-Palsa MJ; Pierre P; Worth RG; Pizza FX. 2013. Skeletal muscle cells express ICAM-1 after muscle overload and ICAM-1 contributes to the ensuing hypertrophic response. PLoS One 8(3):e58486. [PubMed: 23505517]  [MGI Ref ID J:199925]

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]

Gatzka M; Hainzl A; Peters T; Singh K; Tasdogan A; Wlaschek M; Scharffetter-Kochanek K. 2013. Reduction of CD18 promotes expansion of inflammatory gammadelta T cells collaborating with CD4+ T cells in chronic murine psoriasiform dermatitis. J Immunol 191(11):5477-88. [PubMed: 24190659]  [MGI Ref ID J:207148]

Gudjonsson JE; Johnston A; Dyson M; Valdimarsson H; Elder JT. 2007. Mouse models of psoriasis. J Invest Dermatol 127(6):1292-308. [PubMed: 17429444]  [MGI Ref ID J:121548]

Guerau-de-Arellano M; Alroy J; Huber BT. 2005. Beta2 integrins control the severity of murine Lyme carditis. Infect Immun 73(6):3242-50. [PubMed: 15908348]  [MGI Ref ID J:99145]

Gujral JS; Farhood A; Bajt ML; Jaeschke H. 2003. Neutrophils aggravate acute liver injury during obstructive cholestasis in bile duct-ligated mice. Hepatology 38(2):355-63. [PubMed: 12883479]  [MGI Ref ID J:105960]

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]

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]

Jones SP; Trocha SD; Strange MB; Granger DN; Kevil CG; Bullard DC; Lefer DJ. 2000. Leukocyte and endothelial cell adhesion molecules in a chronic murine model of myocardial reperfusion injury Am J Physiol Heart Circ Physiol 279(5):H2196-201. [PubMed: 11045953]  [MGI Ref ID J:65658]

Joussen AM; Poulaki V; Le ML; Koizumi K; Esser C; Janicki H; Schraermeyer U; Kociok N; Fauser S; Kirchhof B; Kern TS; Adamis AP. 2004. A central role for inflammation in the pathogenesis of diabetic retinopathy. FASEB J 18(12):1450-2. [PubMed: 15231732]  [MGI Ref ID J:118466]

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]

Kess D; Lindqvist AK; Peters T; Wang H; Zamek J; Nischt R; Broman KW; Blakytny R; Krieg T; Holmdahl R; Scharffetter-Kochanek K. 2006. Identification of susceptibility loci for skin disease in a murine psoriasis model. J Immunol 177(7):4612-9. [PubMed: 16982899]  [MGI Ref ID J:117544]

Kess D; Peters T; Zamek J; Wickenhauser C; Tawadros S; Loser K; Varga G; Grabbe S; Nischt R; Sunderkotter C; Muller W; Krieg T; Scharffetter-Kochanek K. 2003. CD4+ T cell-associated pathophysiology critically depends on CD18 gene dose effects in a murine model of psoriasis. J Immunol 171(11):5697-706. [PubMed: 14634077]  [MGI Ref ID J:109598]

Kodali P; Wu P; Lahiji PA; Brown EJ; Maher JJ. 2006. ANIT toxicity toward mouse hepatocytes in vivo is mediated primarily by neutrophils via CD18. Am J Physiol Gastrointest Liver Physiol 291(2):G355-63. [PubMed: 16614373]  [MGI Ref ID J:112906]

Lammermann T; Afonso PV; Angermann BR; Wang JM; Kastenmuller W; Parent CA; Germain RN. 2013. Neutrophil swarms require LTB4 and integrins at sites of cell death in vivo. Nature 498(7454):371-5. [PubMed: 23708969]  [MGI Ref ID J:198733]

Lejtenyi D; Osmond DG; Miller SC. 2003. Natural killer cells and B lymphocytes in L-selectin and Mac-1/LFA-1 knockout mice: marker-dependent, but not cell lineage-dependent changes in the spleen and bone marrow. Immunobiology 207(2):129-35. [PubMed: 12675270]  [MGI Ref ID J:102758]

Looney MR; Nguyen JX; Hu Y; Van Ziffle JA; Lowell CA; Matthay MA. 2009. Platelet depletion and aspirin treatment protect mice in a two-event model of transfusion-related acute lung injury. J Clin Invest 119(11):3450-61. [PubMed: 19809160]  [MGI Ref ID J:154615]

Marino JS; Tausch BJ; Dearth CL; Manacci MV; McLoughlin TJ; Rakyta SJ; Linsenmayer MP; Pizza FX. 2008. Beta2-integrins contribute to skeletal muscle hypertrophy in mice. Am J Physiol Cell Physiol 295(4):C1026-36. [PubMed: 18753316]  [MGI Ref ID J:142465]

Matynia A; Anagnostaras SG; Wiltgen BJ; Lacuesta M; Fanselow MS; Silva AJ. 2008. A high through-put reverse genetic screen identifies two genes involved in remote memory in mice. PLoS ONE 3(5):e2121. [PubMed: 18464936]  [MGI Ref ID J:136217]

Merched A; Tollefson K; Chan L. 2010. Beta2 integrins modulate the initiation and progression of atherosclerosis in low-density lipoprotein receptor knockout mice. Cardiovasc Res 85(4):853-63. [PubMed: 19843511]  [MGI Ref ID J:172548]

Nakao S; Zandi S; Faez S; Kohno R; Hafezi-Moghadam A. 2012. Discontinuous LYVE-1 expression in corneal limbal lymphatics: dual function as microvalves and immunological hot spots. FASEB J 26(2):808-17. [PubMed: 22090317]  [MGI Ref ID J:180605]

Oldenborg PA; Gresham HD; Lindberg FP. 2001. CD47-signal regulatory protein alpha (SIRPalpha) regulates Fcgamma and complement receptor-mediated phagocytosis. J Exp Med 193(7):855-62. [PubMed: 11283158]  [MGI Ref ID J:120547]

Papayannopoulou T; Priestley GV; Nakamoto B; Zafiropoulos V; Scott LM; Harlan JM. 2001. Synergistic mobilization of hemopoietic progenitor cells using concurrent beta1 and beta2 integrin blockade or beta2-deficient mice. Blood 97(5):1282-8. [PubMed: 11222371]  [MGI Ref ID J:67767]

Sakurai E; Taguchi H; Anand A; Ambati BK; Gragoudas ES; Miller JW; Adamis AP; Ambati J. 2003. Targeted disruption of the CD18 or ICAM-1 gene inhibits choroidal neovascularization. Invest Ophthalmol Vis Sci 44(6):2743-9. [PubMed: 12766082]  [MGI Ref ID J:119416]

Scott MJ; Billiar TR. 2008. Beta2-integrin-induced p38 MAPK activation is a key mediator in the CD14/TLR4/MD2-dependent uptake of lipopolysaccharide by hepatocytes. J Biol Chem 283(43):29433-46. [PubMed: 18701460]  [MGI Ref ID J:142561]

Smith E; Zarbock A; Stark MA; Burcin TL; Bruce AC; Foley P; Ley K. 2007. IL-23 is required for neutrophil homeostasis in normal and neutrophilic mice. J Immunol 179(12):8274-9. [PubMed: 18056371]  [MGI Ref ID J:155034]

Sorgi CA; Secatto A; Fontanari C; Turato WM; Belanger C; de Medeiros AI; Kashima S; Marleau S; Covas DT; Bozza PT; Faccioli LH. 2009. Histoplasma capsulatum cell wall {beta}-glucan induces lipid body formation through CD18, TLR2, and dectin-1 receptors: correlation with leukotriene B4 generation and role in HIV-1 infection. J Immunol 182(7):4025-35. [PubMed: 19299700]  [MGI Ref ID J:147134]

Sumagin R; Lomakina E; Sarelius IH. 2008. Leukocyte-endothelial cell interactions are linked to vascular permeability via ICAM-1-mediated signaling. Am J Physiol Heart Circ Physiol 295(3):H969-H977. [PubMed: 18641276]  [MGI Ref ID J:141283]

Taylor PR; Roy S; Leal SM Jr; Sun Y; Howell SJ; Cobb BA; Li X; Pearlman E. 2014. Activation of neutrophils by autocrine IL-17A-IL-17RC interactions during fungal infection is regulated by IL-6, IL-23, RORgammat and dectin-2. Nat Immunol 15(2):143-51. [PubMed: 24362892]  [MGI Ref ID J:209279]

Tu L; Poe JC; Kadono T; Venturi GM; Bullard DC; Tedder TF; Steeber DA. 2002. A functional role for circulating mouse L-selectin in regulating leukocyte/endothelial cell interactions in vivo. J Immunol 169(4):2034-43. [PubMed: 12165530]  [MGI Ref ID J:120206]

Wang H; Kess D; Lindqvist AK; Peters T; Sindrilaru A; Wlaschek M; Blakytny R; Holmdahl R; Scharffetter-Kochanek K. 2008. A 9-centimorgan interval of chromosome 10 controls the T cell-dependent psoriasiform skin disease and arthritis in a murine psoriasis model. J Immunol 180(8):5520-9. [PubMed: 18390736]  [MGI Ref ID J:134251]

Wang H; Peters T; Kess D; Sindrilaru A; Oreshkova T; Van Rooijen N; Stratis A; Renkl AC; Sunderkotter C; Wlaschek M; Haase I; Scharffetter-Kochanek K. 2006. Activated macrophages are essential in a murine model for T cell-mediated chronic psoriasiform skin inflammation. J Clin Invest 116(8):2105-14. [PubMed: 16886059]  [MGI Ref ID J:113121]

Wang H; Peters T; Sindrilaru A; Kess D; Oreshkova T; Yu XZ; Seier AM; Schreiber H; Wlaschek M; Blakytny R; Rohrbein J; Schulz G; Weiss JM; Scharffetter-Kochanek K. 2008. TGF-beta-dependent suppressive function of Tregs requires wild-type levels of CD18 in a mouse model of psoriasis. J Clin Invest 118(7):2629-39. [PubMed: 18521187]  [MGI Ref ID J:137678]

Wang H; Syrovets T; Kess D; Buchele B; Hainzl H; Lunov O; Weiss JM; Scharffetter-Kochanek K; Simmet T. 2009. Targeting NF-kappaB with a natural triterpenoid alleviates skin inflammation in a mouse model of psoriasis. J Immunol 183(7):4755-63. [PubMed: 19752240]  [MGI Ref ID J:152764]

Wang H; von Rohrscheidt J; Roehrbein J; Peters T; Sindrilaru A; Kess D; Preissner KT; Scharffetter-Kochanek K. 2010. Extracellular adherence protein of Staphylococcus aureus suppresses disease by inhibiting T-cell recruitment in a mouse model of psoriasis. J Invest Dermatol 130(3):743-54. [PubMed: 19812597]  [MGI Ref ID J:159562]

Wang L; Gordon RA; Huynh L; Su X; Park Min KH; Han J; Arthur JS; Kalliolias GD; Ivashkiv LB. 2010. Indirect inhibition of Toll-like receptor and type I interferon responses by ITAM-coupled receptors and integrins. Immunity 32(4):518-30. [PubMed: 20362473]  [MGI Ref ID J:160755]

Weckbach LT; Gola A; Winkelmann M; Jakob SM; Groesser L; Borgolte J; Pogoda F; Pick R; Pruenster M; Muller-Hocker J; Deindl E; Sperandio M; Walzog B. 2014. The cytokine midkine supports neutrophil trafficking during acute inflammation by promoting adhesion via beta2 integrins (CD11/CD18). Blood 123(12):1887-96. [PubMed: 24458438]  [MGI Ref ID J:209651]

Wu X; Guo R; Wang Y; Cunningham PN. 2007. The role of ICAM-1 in endotoxin-induced acute renal failure. Am J Physiol Renal Physiol 293(4):F1262-71. [PubMed: 17670897]  [MGI Ref ID J:145124]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryThe Itgb2tm1Bay strain is maintained by homozygous sibling matings. Homozygous mice may be ordered. Expected coat color from breeding:Black
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHomozygous for Itgb2tm1Bay  
Price per Pair (US dollars $)Pair Genotype
$399.80Homozygous for Itgb2tm1Bay x Homozygous for Itgb2tm1Bay  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHomozygous for Itgb2tm1Bay  
Price per Pair (US dollars $)Pair Genotype
$519.80Homozygous for Itgb2tm1Bay x Homozygous for Itgb2tm1Bay  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice
Surgical and Preconditioning Services
JAX® Services
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Tel: 1-800-422-6423 or 1-207-288-5845
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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