Phenotypes associated with this allele

• Allele Symbol: Itgam^tm1Bll
• Allele Name: targeted mutation 1, Christie M Ballantyne
• Allele ID: MGI:2157556
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Itgam^tm1Bll/Itgam^tm1Bll	B6.129S7-Itgam^tm1Bll	MGI:3583099
hm2	Itgam^tm1Bll/Itgam^tm1Bll	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3583151

Genotype
MGI:3583099

hm1

• Allelic Composition: Itgam^tm1Bll/Itgam^tm1Bll
• Genetic Background: B6.129S7-Itgam^tm1Bll

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

immune system

abnormal leukocyte adhesion ( J:100242 )

• leukocyte adhesion efficiency in inflamed vessels is significantly reduced from that in wildtype, is significantly increased compared with that of homozygous Itgal^tm1Bll mice, and similar to that of homozygous Icam1^tm1Alb mice

• 52% of leukocytes adhere to endothelium compared to 95% in wildtype

abnormal lymphocyte cell number ( J:90954 )

• SEA injection induced less of a decrease in the numbers of thymocytes than in wild-type

abnormal T cell subpopulation ratio ( J:90954 )

• significantly lower ratio of CD4+ to CD8+ cells in splenocytes and thymocytes

decreased CD4-positive, alpha-beta T cell number ( J:90954 )

• decreased numbers of CD4+ cells in splenocytes and thymocytes

increased CD8-positive, alpha-beta T cell number ( J:90954 )

• increased numbers of CD8+ cells in splenocytes and thymocytes

increased leukocyte cell number ( J:100242 )

• total leukocyte numbers, polymophonuclear cell numbers and mononuclear cell numbers are increased

increased neutrophil cell number ( J:100242 )

• 4-fold increase in the number of circulating neutrophils

abnormal T cell activation ( J:90954 )

• splenocytes responded poorly to PHA and ConA stimulation, indicating poor T cell activation

decreased T cell proliferation ( J:90954 )

• reduced staphylococcal enterotoxin A, B or E (SEA, SEB, SEE)-induced T cell proliferation in splenocytes compared to wild-type and was even more decreased than in homozygous Itgal mutant mice

increased susceptibility to bacterial infection ( J:94855 )

• mice are more susceptible to pneumococcal infection than controls

• when challenged with a PspA⁺ bacterial strain, 88% of mice die within 72 hours compared to 58% of wild-type mice

• when challenged with a PspA^- bacterial strain, mice have a 10-fold higher burden 4 hours after infection

• mice on average die 3.5 days after infection compared to none in wild-type controls

hematopoietic system

abnormal leukocyte adhesion ( J:100242 )

• leukocyte adhesion efficiency in inflamed vessels is significantly reduced from that in wildtype, is significantly increased compared with that of homozygous Itgal^tm1Bll mice, and similar to that of homozygous Icam1^tm1Alb mice

• 52% of leukocytes adhere to endothelium compared to 95% in wildtype

abnormal lymphocyte cell number ( J:90954 )

• SEA injection induced less of a decrease in the numbers of thymocytes than in wild-type

abnormal T cell subpopulation ratio ( J:90954 )

• significantly lower ratio of CD4+ to CD8+ cells in splenocytes and thymocytes

decreased CD4-positive, alpha-beta T cell number ( J:90954 )

• decreased numbers of CD4+ cells in splenocytes and thymocytes

increased CD8-positive, alpha-beta T cell number ( J:90954 )

• increased numbers of CD8+ cells in splenocytes and thymocytes

increased leukocyte cell number ( J:100242 )

• total leukocyte numbers, polymophonuclear cell numbers and mononuclear cell numbers are increased

increased neutrophil cell number ( J:100242 )

• 4-fold increase in the number of circulating neutrophils

abnormal T cell activation ( J:90954 )

• splenocytes responded poorly to PHA and ConA stimulation, indicating poor T cell activation

decreased T cell proliferation ( J:90954 )

• reduced staphylococcal enterotoxin A, B or E (SEA, SEB, SEE)-induced T cell proliferation in splenocytes compared to wild-type and was even more decreased than in homozygous Itgal mutant mice

cellular

abnormal leukocyte adhesion ( J:100242 )

• leukocyte adhesion efficiency in inflamed vessels is significantly reduced from that in wildtype, is significantly increased compared with that of homozygous Itgal^tm1Bll mice, and similar to that of homozygous Icam1^tm1Alb mice

• 52% of leukocytes adhere to endothelium compared to 95% in wildtype

decreased T cell proliferation ( J:90954 )

• reduced staphylococcal enterotoxin A, B or E (SEA, SEB, SEE)-induced T cell proliferation in splenocytes compared to wild-type and was even more decreased than in homozygous Itgal mutant mice

Genotype
MGI:3583151

hm2

• Allelic Composition: Itgam^tm1Bll/Itgam^tm1Bll
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

immune system

abnormal leukocyte migration ( J:83226 )

• leukocyte influx in a subcutaneous air pouch in response to TNF-alpha is increased by 198%

abnormal cellular extravasation ( J:83226 )

• neutrophil extravasation in response to TNF-alpha is increased

abnormal leukocyte adhesion ( J:83226 )

• adhesion of neutrophils to ICAM-1 or endothelial cells is increased with Zas stimulation but not to the same extent as in wild-type neutrophils

• adhesion of neutrophils to fibrinogen and KLH is completely abolished

• neutrophils show a decrease in adhesion in response to shear stress, but to a lesser extent than seen in Itgb2^tm2Bay or Itgal^tm1Bll mice

decreased eosinophil cell number ( J:83226 )

abnormal neutrophil physiology ( J:39092 )

• neutrophils exhibited greater than 90% reduction in adhesion to fibrinogen-coated disks, defective adhesion to keyhole limpet hemocyanin-coated glass, defective homotypic aggregation, and reduced degranulation, however neutrophil emigration in the peritoneal cavity after thioglycollate challenge was normal

impaired neutrophil phagocytosis ( J:39092 )

• showed defective iC3b-mediated phagocytosis

hematopoietic system

abnormal leukocyte migration ( J:83226 )

• leukocyte influx in a subcutaneous air pouch in response to TNF-alpha is increased by 198%

abnormal cellular extravasation ( J:83226 )

• neutrophil extravasation in response to TNF-alpha is increased

abnormal leukocyte adhesion ( J:83226 )

• adhesion of neutrophils to ICAM-1 or endothelial cells is increased with Zas stimulation but not to the same extent as in wild-type neutrophils

• adhesion of neutrophils to fibrinogen and KLH is completely abolished

• neutrophils show a decrease in adhesion in response to shear stress, but to a lesser extent than seen in Itgb2^tm2Bay or Itgal^tm1Bll mice

decreased eosinophil cell number ( J:83226 )

abnormal neutrophil physiology ( J:39092 )

• neutrophils exhibited greater than 90% reduction in adhesion to fibrinogen-coated disks, defective adhesion to keyhole limpet hemocyanin-coated glass, defective homotypic aggregation, and reduced degranulation, however neutrophil emigration in the peritoneal cavity after thioglycollate challenge was normal

impaired neutrophil phagocytosis ( J:39092 )

• showed defective iC3b-mediated phagocytosis

cellular

abnormal leukocyte migration ( J:83226 )

• leukocyte influx in a subcutaneous air pouch in response to TNF-alpha is increased by 198%

abnormal cellular extravasation ( J:83226 )

• neutrophil extravasation in response to TNF-alpha is increased

abnormal leukocyte adhesion ( J:83226 )

• adhesion of neutrophils to ICAM-1 or endothelial cells is increased with Zas stimulation but not to the same extent as in wild-type neutrophils

• adhesion of neutrophils to fibrinogen and KLH is completely abolished

• neutrophils show a decrease in adhesion in response to shear stress, but to a lesser extent than seen in Itgb2^tm2Bay or Itgal^tm1Bll mice

impaired neutrophil phagocytosis ( J:39092 )

• showed defective iC3b-mediated phagocytosis