Analysis Tools
normal phenotype
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• mice are fertile, develop normally, generate normal immune responses and do not appear to have any evidence of spontaneous pathology
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Allele Symbol Allele Name Allele ID |
Tg(FCGR2A)11Mkz transgene insertion 11, Steven E McKenzie MGI:3056729 |
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| Summary |
4 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are fertile, develop normally, generate normal immune responses and do not appear to have any evidence of spontaneous pathology
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following treatment with KKO and heparin, 2 of 4 mice die unlike similarly treated single transgenic mice
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• following treatment with KKO and heparin
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• following treatment with KKO and heparin, mice exhibit fibrin thrombi in the arterioles and capillaries in the heart, liver, lungs, and kidney unlike similarly treated single transgenic mice
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• following treatment with KKO and heparin
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• following treatment with KKO and heparin
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• following treatment with KKO and heparin
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• following treatment with KKO and heparin
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• following treatment with KKO and heparin, mice exhibit severe thrombopenia, decreased activity, rapid shallow breathing, hunched posture, and tactile hypothermia with increased lethality and fibrin thrombi in the arterioles and capillaries in the heart, liver, lungs, and kidney compared with similarly treated single transgenic mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| acquired thrombocytopenia | DOID:11126 | J:72220 | ||
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• sera IgG2a levels are elevated more than 2-fold in mice with severe spontaneous arthritis
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• macrophages produce 6.5-fold more TNF in response to immunoglobulin aggregates compared to controls
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• macrophages produce 6.5-fold more TNF in response to immunoglobulin aggregates compared to controls
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• in mice over 20 weeks of age, 13 of 23 have anti-histone antibodies above background levels
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• 32% of mice develop a spontaneous form of arthritis between 20 and 50 weeks of age
• arthritis is characterized by severe ankylosis of the tibiotarsal and tarsophalangeal cartilage, loss of joint space and prominent periarticular new bone formation
• the arthritic joints contain synovial hyperplasia and proliferation, cartilage erosion, pannus formation, and joint space infiltrate
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• transgenic mice have an earlier onset of collagen-induced arthritis than controls despite having a protective H2 locus
• mean day of onset is 18 days versus 22 days in the susceptible DBA/1 strain
• 15% of mice develop arthritis with just one immunization of collagen compared to none in DBA/1 mice
• over 90% of mice develop arthritis within six days after a second injection of collagen compared to less then 10% of DBA/1 mice
• mice are also highly susceptible to an arthritis model initiated by injections of anti-collagen antibodies
• 100% of mice develop arthritis after injection of anti-collagen antibody while controls needed an LPS adjuvant in addition to the immunoglobulins to develop disease
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• mice have an age-related progression to severe glomerulonephritis
• few mice have the disease prior to 20 weeks of age, up to 80% have disease by 40 weeks of age, and all mice have disease over 40 weeks of age
• disease is first evident as multifocallymphoplasmacytic infiltrate in the renal interstitium mainly around major arcuate vessels
• more advanced disease was seen, with enlarged glomeruli, increased mesangial matrix and condensation of glomerular tufts
• disease is self-limiting as kidney function is never impaired
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• pneumonitis was found in 25% of mice between 12 to 40 weeks of age and increases to 100% in older mice
• disease is characterized by patches of perivascular inflammation with cellular aggregates of macrophages, lymphocytes, and plasma cells within alveolar walls
• in severe cases, up to 50% of the normal architecture of the lungs is obliterated
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• mice have an age-related progression to severe glomerulonephritis
• few mice have the disease prior to 20 weeks of age, up to 80% have disease by 40 weeks of age, and all mice have disease over 40 weeks of age
• disease is first evident as multifocallymphoplasmacytic infiltrate in the renal interstitium mainly around major arcuate vessels
• more advanced disease was seen, with enlarged glomeruli, increased mesangial matrix and condensation of glomerular tufts
• disease is self-limiting as kidney function is never impaired
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• immunoglobulin deposition is noted in the kidney
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• pneumonitis was found in 25% of mice between 12 to 40 weeks of age and increases to 100% in older mice
• disease is characterized by patches of perivascular inflammation with cellular aggregates of macrophages, lymphocytes, and plasma cells within alveolar walls
• in severe cases, up to 50% of the normal architecture of the lungs is obliterated
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• 32% of mice develop a spontaneous form of arthritis between 20 and 50 weeks of age
• arthritis is characterized by severe ankylosis of the tibiotarsal and tarsophalangeal cartilage, loss of joint space and prominent periarticular new bone formation
• the arthritic joints contain synovial hyperplasia and proliferation, cartilage erosion, pannus formation, and joint space infiltrate
|
|
• transgenic mice have an earlier onset of collagen-induced arthritis than controls despite having a protective H2 locus
• mean day of onset is 18 days versus 22 days in the susceptible DBA/1 strain
• 15% of mice develop arthritis with just one immunization of collagen compared to none in DBA/1 mice
• over 90% of mice develop arthritis within six days after a second injection of collagen compared to less then 10% of DBA/1 mice
• mice are also highly susceptible to an arthritis model initiated by injections of anti-collagen antibodies
• 100% of mice develop arthritis after injection of anti-collagen antibody while controls needed an LPS adjuvant in addition to the immunoglobulins to develop disease
|
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• sera IgG2a levels are elevated more than 2-fold in mice with severe spontaneous arthritis
|
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• macrophages produce 6.5-fold more TNF in response to immunoglobulin aggregates compared to controls
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| rheumatoid arthritis | DOID:7148 |
OMIM:180300 |
J:136516 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• severe thrombocytopenia can be induced in mice by an anti-platelet rat monoclonal antibody specific for platelets that normally induces only a mild thrombocytopenia in wild-type mice
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/30/2024 MGI 6.23 |
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