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Allele Symbol Allele Name Allele ID |
Lyz2tm1(cre)Ifo targeted mutation 1, Irmgard Forster MGI:1934631 |
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| Summary |
174 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• rare
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• rare
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• rare
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in LPS-treated mice
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• LPS-treated mice exhibit increased survival compared with similarly treated wild-type mice
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• in LPS-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fewer capillaries per muscle fiber in gastrocnemius after induced hind limb ischemia
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• reduced microvessel formation in sterile sponges implanted subdermally
• reduced VEGF and MMP-9 in sterile sponges implanted subdermally
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• considerable attenuation of blood flow in the gastrocnemius after induced hind limb ischemia
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• higher level of necrosis in the paws of the hind limb at 2 weeks after induced hind limb ischemia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in response to LPS treatment, mice exhibit increased lethality compared with control mice
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| N |
• mice exhibit normal myelopoiesis
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• enhanced in response to CCR2 signals
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• DSS-treated mice exhibit enhanced progression and maintenance of inflammatory colitis and 2 of 19 mice develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
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• in response to LPS treatment
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• in response to LPS treatment
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• in response to LPS treatment
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• in response to LPS treatment
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• in response to LPS treatment, mice exhibit increased lethality and increased serum levels of TNF, IL6, IL1B and IL12 compared with control mice
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• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
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• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
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• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
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• in mice treated with DSS and DMH
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• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
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• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
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• DSS-treated mice exhibit enhanced progression and maintenance of inflammatory colitis and 2 of 19 mice develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
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• in response to LPS treatment
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• in response to LPS treatment
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• in response to LPS treatment
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• in response to LPS treatment
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• in response to LPS treatment, mice exhibit increased lethality compared with control mice
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• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
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• enhanced in response to CCR2 signals
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• enhanced in response to CCR2 signals
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal susceptibility to MOG induced experimental autoimmune encephalomyelitis and response to treatment with dexamethasone
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in a CASP model of septic peritonitis, mice exhibit reduced circulating CXCL1 compared with control mice
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• in a model of septic peritonitis
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• in a model of septic peritonitis
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• in a model of septic peritonitis
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• in response to septic peritonitis, the peritoneal lavage fluid contains less CXCL10 compared with control mice
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• in a model of septic peritonitis, mice exhibit aggravated liver injury compared with control mice
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| N |
• mice exhibit normal expression of cytokines and neutrophil accumulation in inflammatory models
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• in a CASP model of septic peritonitis, mice exhibit reduced circulating CXCL1 compared with control mice
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• in a model of septic peritonitis
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• in response to septic peritonitis, the peritoneal lavage fluid contains less CXCL10 compared with control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in mice infected with K. pneumonia
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• following cecal ligation and puncture
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• in mice infected with K. pneumonia or following cecal ligation and puncture
• however, response to S. aureus is normal
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• in mice infected with K. pneumonia or following cecal ligation and puncture
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• in peritoneal macrophages from mice stimulated with LPS or K. pneumonia
• however, response to LTA and S. aureus is normal
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• mice infected with K. pneumonia exhibit improved survival, decreased circulating levels of IL6 and TNFalpha, decreased bacterial dissemination and increased neutrophil infiltration compared with control mice
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• in mice infected with K. pneumonia
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• in mice infected with K. pneumonia or following cecal ligation and puncture
• however, response to S. aureus is normal
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• in mice infected with K. pneumonia or following cecal ligation and puncture
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• following cecal ligation and puncture, mice exhibit improved survival, decreased circulating levels of IL6 and TNFalpha, decreased bacterial dissemination and increased neutrophil infiltration compared with control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are resistant to the wasting disease caused by systemic infection with T. gondii
• control mice lose 20% of their body weight by 40 days after T. gondii infection while infected mutant mice have no loss of body weight
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal development and distribution of NK T cells
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• decreased in splenic and liver NK cells after injection of alphaGC
• decreased in splenic NK T cells after injection of alphaGC
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• decreased in splenic and liver NK T cells after injection of alphaGC
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• inguinal adipocytes are smaller in size than controls
• however, in mice fed high fat diet (HFD) the size of visceral adipocytes is similar in both mutant and controls
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• increased amount of epididymal fat
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• HFD-fed mice do not exhibit an impaired freeze response in the fear conditioning assay unlike HFD-fed controls
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• decrease in crown-like structures formed by macrophages in visceral adipose tissue of mice fed HFD as compared to HFD-fed controls
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• decrease in body weight in 5-7 month old mice as compared to controls
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• decrease in snout-anus length
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• delay in fat accumulation on high fat diet (HFD) as compared to controls
• delay in relative loss of lean mass in first 6 weeks of HFD
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• decrease in crown-like structures formed by macrophages in visceral adipose tissue of mice fed HFD as compared to HFD-fed controls
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• delay in fat accumulation on high fat diet (HFD) as compared to controls
• delay in relative loss of lean mass in first 6 weeks of HFD
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• glucose levels are lower in HFD-fed mice as compared to HFD-fed controls
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• insulin levels are lower in HFD-fed mice as compared to HFD-fed controls
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• HDL levels are increased in HFD-fed mice as compared to HFD-fed controls
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• total cholesterol levels are lower in both HFD-fed mice and CD-fed mice as compared to controls
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• LDL cholesterol levels are lower in HFD-fed mice as compared to HFD-fed controls
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• triglyceride levels are lower in HFD-fed mice as compared to HFD-fed controls
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• decrease in crown-like structures formed by macrophages in visceral adipose tissue of mice fed HFD as compared to HFD-fed controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice treated with DSS exhibit a slight reduction of colitis in the early phase compared with control mice
• however, there is no protection after 9 days
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| N |
• mice treated with azoxymethane and dextran sulfate sodium exhibit normal tumorigenesis
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• mice treated with DSS exhibit a slight reduction of colitis in the early phase compared with control mice
• however, there is no protection after 9 days
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in mice treated with diphtheria toxin following injection of carrageenan
• treatment with dexamethasone does not prevent carrageenan-triggered inflammatory-related mechanical hypersensitivity
|
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• following injection of carrageenan, female and male mice treated with diphtheria toxin exhibit failure to resolve inflammatory mechanical hyperalgesia, thermal hyperalgesia, and posture changes related to inflammatory pain compared with control mice
• mice treated with diphtheria toxin fail to resolve complete Freunds adjuvant-induced transient inflammatory hyperalgesia unlike control mice
• treatment with dexamethasone does not prevent carrageenan-triggered inflammatory-related mechanical hypersensitivity
• macrophages lacking Il4ra, Stat6, or Cd200r1 fail to resolve inflammatory hyperalgesia
• however, carrageenan-induced inflammation is resolved in diphtheria toxin-treated mice and hyperalgesia was rescued by injection of in vitro differentiated bone marrow-derived macrophages and macrophages differentiated with IL-4
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• in mice treated with diphtheria toxin following injection of carrageenan
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after stimulation with heat-killed and PI (propidium iodide)-labeled E. coli for 1 h, peritoneal macrophages endocytose significantly less E. coli than controls macrophages; endocytosed E. coli do not colocalize with Cav1, unlike in control macrophages
• 1 h after infection macrophages show significantly less endocytosis of viable E. coli or S. aureus than control macrophages, as measured by CFUs
• after incubation with Zymosan or latex beads, mean fluorescence intensity of bone marrow-derived macrophages (BMDMs) is significantly lower than that of control macrophages
• upon LPS stimulation, % of surface TLR4 on BMDMs is significantly higher than that on control macrophages, indicating impaired LPS-activated endocytosis of TLR4
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• after exposure to E. coli, the % of live E. coli counts to initially internalized counts is significantly higher than that in control macrophages, suggesting that bactericidal capacity of macrophages is impaired
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• serum IFN-beta levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
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• serum IL-6 levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
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• serum TNFalpha levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
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• upon E. coli or LPS challenge, mice show significantly reduced production of the inflammatory cytokines TNFalpha, IFN-beta, and IL-6 in serum relative to control mice
• upon E. coli or LPS stimulation, macrophages show deceased production of TNFalpha, IFN-beta, and IL-6 relative to control macrophages
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• mice are more susceptible to i.p. E. coli infection with significantly higher bacterial loads in spleen and liver, reduced production of TNFalpha, IFN-beta, and IL-6 in serum, and decreased infiltration of inflammatory cells in lung relative to similarly infected control mice
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• after i.p. injection with E. coli, all mice die by 3 days after challenge whereas most control mice survive to 5 days post infection
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• serum IFN-beta levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
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• serum IL-6 levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
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• serum TNFalpha levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
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• after exposure to E. coli, the % of live E. coli counts to initially internalized counts is significantly higher than that in control macrophages, suggesting that bactericidal capacity of macrophages is impaired
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• after i.p. injection with E. coli, all mice die by 3 days after challenge whereas most control mice survive to 5 days post infection
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduction in osteoclast formation
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• mice exhibit a decrease in bone formation rate
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• reduction in osteoclast formation
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• reduction in osteoclast formation
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• reduction in osteoclast formation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• chow-fed mice exhibit a slight but significant reduction in lean mass relative to controls
• however, mice fed a high fat diet (HFD) for 4 weeks show no differences in lean mass relative to HFD-fed controls
|
| N |
• chow-fed mice exhibit comparable insulin and glucose tolerance and blood concentrations of glucose and insulin relative to chow-fed controls
• HFD-fed mice show comparable diet-induced obesity with no differences in blood glycerol and free fatty acids (FFA) levels relative to HFD-fed controls
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• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated cytokine levels relative to chow-fed control mice
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• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated chemokine levels relative to chow-fed control mice
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• hyperinsulinemic-euglycemic clamp studies revealed that mice fed either a regular chow or a HFD show a significantly enhanced steady-state glucose infusion rate, clamp hepatic glucose production, and insulin-stimulated whole-body glucose turnover relative to similarly-fed control mice
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• HFD-fed mice show a significant increase in glucose-induced insulin secretion both in vitro and in vivo relative to HFD-fed controls
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• mice are protected from HFD-induced hyperglycemia, unlike HFD-fed controls
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• mice are protected from HFD-induced hyperinsulinemia, unlike HFD-fed controls
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• HFD-fed mice show significantly reduced gluconeogenesis relative to HFD-fed controls
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• HFD-fed mice show improved glucose tolerance relative to HFD-fed controls
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• hyperinsulinemic-euglycemic clamp studies revealed that mice fed either a regular chow or a HFD show a significantly enhanced whole-body glycogen plus lipid synthesis relative to similarly-fed control mice
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• HFD-fed mice show improved insulin tolerance relative to HFD-fed controls
• hyperinsulinemic-euglycemic clamp studies revealed that increased whole-body insulin sensitivity is due to significant improvements in glucose infusion rates, hepatic insulin action, clamp hepatic glucose production, insulin-stimulated whole body glucose turnover, and whole-body glycogen plus lipid synthesis relative to control mice
• after overnight fasting, HFD-fed mice fail to suppress insulin-stimulated Akt activation in the liver, white adipose tissue and skeletal muscle, unlike similarly treated HFD-fed control mice
• protection of HFD-fed mice against insulin resistance is associated with reduced tissue infiltration by macrophages
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• hyperinsulinemic-euglycemic clamp studies revealed that mice fed either a regular chow or a HFD show a significantly enhanced whole-body glycogen plus lipid synthesis relative to similarly-fed control mice
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• HFD-fed mice show significantly reduced chemokine expression relative to HFD-fed controls
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of chemokine (Ccl2 and Ccl5) genes relative to control BMDMs
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• HFD-fed mice show a significant reduction in pancreatic beta cell proliferation relative to HFD-fed controls
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• HFD-fed mice show a significant reduction in pancreatic islet area relative to HFD-fed controls
• however, chow-fed mice show no differences in islet area relative to chow-fed controls
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• HFD-fed mice show a significant increase in glucose-induced insulin secretion both in vitro and in vivo relative to HFD-fed controls
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• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show reduced M1 differentiation and expression of the cell surface marker CD11c relative to control BMDMs
• however, M2 differentiation appears unaffected
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• HFD-fed mice show a significant decrease in the total number of F4/80+ adipose tissue macrophages (ATMs) and reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice also show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• chow-fed mice show no differences in total, M1- or M2-polarized ATM number relative to chow-fed controls
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• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of M1 marker genes (Ccr7 and Cd11c), chemokines (Ccl2 and Ccl5), and cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
• similar defects are detected in LPS-stimulated macrophages
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• HFD-fed mice show significantly reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• however, HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
|
|
• upon IFN-gamma stimulation, isolated BMDMs show decreased expression of cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
|
|
• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated cytokine levels relative to chow-fed control mice
|
|
• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated chemokine levels relative to chow-fed control mice
|
|
• HFD-fed mice show significantly reduced chemokine expression relative to HFD-fed controls
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of chemokine (Ccl2 and Ccl5) genes relative to control BMDMs
|
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• HFD-fed mice show significantly reduced hepatic inflammation relative to HFD-fed controls
|
|
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show reduced M1 differentiation and expression of the cell surface marker CD11c relative to control BMDMs
• however, M2 differentiation appears unaffected
|
|
• HFD-fed mice show a significant decrease in the total number of F4/80+ adipose tissue macrophages (ATMs) and reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice also show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• chow-fed mice show no differences in total, M1- or M2-polarized ATM number relative to chow-fed controls
|
|
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of M1 marker genes (Ccr7 and Cd11c), chemokines (Ccl2 and Ccl5), and cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
• similar defects are detected in LPS-stimulated macrophages
|
|
• HFD-fed mice show significantly reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• however, HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
|
|
• upon IFN-gamma stimulation, isolated BMDMs show decreased expression of cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
|
|
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show reduced M1 differentiation and expression of the cell surface marker CD11c relative to control BMDMs
• however, M2 differentiation appears unaffected
|
|
• HFD-fed mice show significantly reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• however, HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
|
|
• HFD-fed mice show a significant reduction in pancreatic beta cell proliferation relative to HFD-fed controls
|
|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• bone formation rate with prednisolone treatment for 2 weeks is reduced in mutants and controls
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in draining lymph node cells from collagen-treated wild-type mice
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• in draining lymph node cells from collagen-treated wild-type mice
|
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• myeloid cells from collage-treated mice exhibit increased CXCL1 and CXCL2 production compared with wild-type mice
|
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• in draining lymph node cells from collagen-treated wild-type mice
• in myeloid cells from the ankles of collagen-treated mice
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• in myeloid cells from the ankles of collagen-treated mice
|
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• in draining lymph node cells from collagen-treated wild-type mice
• in myeloid cells from the ankles of collagen-treated mice
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• in myeloid cells from the ankles of collage-treated mice
|
|
• collagen treated mice exhibit earlier and more severe arthritis with increased number of paws affected, inflammation, cartilage erosion, and neutrophil infiltration compared with similarly treated wild-type mice
• draining lymph node cells from collagen-stimulated mice exhibit increased T cell proliferation, and IFN-gamma and IL17 production compared with similarly treated wild-type cells
• myeloid cells from the ankles of collagen-treated mice exhibit increased IL1b, IL6, IFNgamma, IL17, CXCL1, and CXCL2 production compared with wild-type mice
|
|
• collagen treated mice exhibit earlier and more severe arthritis with increased number of paws affected, inflammation, cartilage erosion, and neutrophil infiltration compared with similarly treated wild-type mice
• draining lymph node cells from collagen-stimulated mice exhibit increased T cell proliferation, and IFN-gamma and IL17 production compared with similarly treated wild-type cells
• myeloid cells from the ankles of collagen-treated mice exhibit increased IL1b, IL6, IFNgamma, IL17, CXCL1, and CXCL2 production compared with wild-type mice
|
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• in draining lymph node cells from collagen-treated wild-type mice
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|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Hmox1tm1.1Gkl/Hmox1tm1.1Gkl Lyz2tm1(cre)Ifo/Lyz2+ mice show decreased susceptibility to L. monocytogenes infection
|
• mice infected with L. monocytogenes and treated with polyI:C exhibit decreased IFN-beta production and mortality compared to similarly treated wild-type mice
|
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• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
|
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• in MOG-treated mice
|
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• in MOG-treated mice
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• MOG-treated mice exhibit an increase in CD4+ T cells compared to in similarly treated wild-type mice
• MOG-treated mice exhibit a 5-fold increase in the number of IL17-producing CD4+ T cells and a 2-fold increase in IFN-gamma-producing CD4+ T cells compared to similarly treated wild-type mice
|
|
• in MOG-treated mice
|
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• in MOG-treated mice
|
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• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
|
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• polyI:C- or LPS-stimulated macrophages or mice stimulated with LPS and infected with L. monocytogenes produce less IFN-beta than similarly treated wild-type cells or mice
• macrophages infected with the Sendai virus produce less IFN-beta than similarly treated wild-type cells
|
|
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
|
|
• mice exhibit exacerbated experimental autoimmune encephalomyelitis (EAE) and do not exhibit suppression of EAE symptoms and IFN-beta production by polyI:C treatment unlike similarly treated wild-type mice
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
• MOG-treated mice exhibit more cellular infiltration with increased CD4+ and CD8+ T cells, macrophages, B cells, and granulocytes and increased demyelination throughout the spinal cord compared to similarly treated wild-type mice
• MOG-treated mice exhibit a 5-fold increase in the number of IL17-producing CD4+ T cells and a 2-fold increase in IFN-gamma-producing CD4+ T cells compared to similarly treated wild-type mice
|
|
• mice infected with L. monocytogenes and treated with polyI:C exhibit decreased IFN-beta production and mortality compared to similarly treated wild-type mice
|
|
• macrophages infected with the Sendai virus produce less IFN-beta than similarly treated wild-type cells
|
|
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
|
|
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
|
|
• in MOG-treated mice
|
|
• in MOG-treated mice
|
|
• MOG-treated mice exhibit an increase in CD4+ T cells compared to in similarly treated wild-type mice
• MOG-treated mice exhibit a 5-fold increase in the number of IL17-producing CD4+ T cells and a 2-fold increase in IFN-gamma-producing CD4+ T cells compared to similarly treated wild-type mice
|
|
• in MOG-treated mice
|
|
• in MOG-treated mice
|
|
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after renal ischemia-reperfusion experiments
|
|
• increased degranulation
|
|
• increased degranulation
|
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• in serum after renal ischemia-reperfusion experiments
|
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• increased degranulation
|
|
• increased degranulation
|
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• after renal ischemia-reperfusion experiments
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants infected with Listeria monocytogenes developed large, confluent inflammatory necrotic areas with many Mac-1 and Gr1-positive cells
• no liver necrosis, only infiltrating cells, were detected in mutants with ConA induced autoimmune hepatitis
|
|
• died within 4 days after Listeria monocytogenes infection whereas controls survived
|
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• serum TNF levels were dramatically reduced in mutants injected with LPS, with TNF production decreased by 100-fold in macrophages
|
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• induction of MCP-1 was reduced in spleens of mutants infected with Listeria monocytogenes
|
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• increased resistance to liver injury after ConA-induced autoimmune hepatitis
|
|
• fully resistant to lipopolysaccharide (LPS)/D-Gal induced septic shock
• protected from toxic shock induced by enterotoxin B, a superantigen from S. aureus
|
|
• loss of resistance against Listeria monocytogenes, developing uncontrolled infection, leading to death within 4 days and a 3-4 log increase in bacterial load in the liver and spleen
|
|
• mutants infected with Listeria monocytogenes developed large, confluent inflammatory necrotic areas with many Mac-1 and Gr1-positive cells
• no liver necrosis, only infiltrating cells, were detected in mutants with ConA induced autoimmune hepatitis
|
|
• serum TNF levels were dramatically reduced in mutants injected with LPS, with TNF production decreased by 100-fold in macrophages
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• no elevation of expression of major histocompatibility complex (MHC) class II peptides on surface of resident peritoneal macrophages
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• LPS-induced alternative pathway (AP) complement activation is impaired unlike in wild-type mice
|
|
|
• in a K/BxN model
|
|
|
• in a K/BxN model
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice treated with dextran sodium sulfate (DSS) to induce colitis show similar colitis-induced injury as controls, with slightly greater weight loss but similar colon shortening and splenic enlargement
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants are more resistant to LPS induced endotoxin shock
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice appear phenotypically normal and do not develop the inflammatory disease that conditional heterozygotes develop on an intact Pycard background
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• postnatal lethality does not occur to mice on a IL-1 receptor null background
|
|
• variable skin inflammation is observed
|
|
• variable skin inflammation is observed
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• following wire injury, mice exhibit decreased intima to media ratio and stenosis percent with increased leukocyte recruitment compared with control mice
|
|
• decreased LPS-stimulated prostaglandin E2
• however, LPS-stimulated prostaglandin D2 levels are normal
|
|
• increased LPS-stimulated prostaglandin I2 levels
|
|
• increased leukocyte recruitment following wire injury
|
|
• increased leukocyte recruitment following wire injury
|
|
• following wire injury, mice exhibit decreased intima to media ratio and stenosis percent with increased leukocyte recruitment compared with control mice
|
|
• increased leukocyte recruitment following wire injury
|
|
• increased leukocyte recruitment following wire injury
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice die between 2 and 14 days after birth probably due to multisystem organ failure secondary to inflammation and necrosis
• genotype demonstrates inflammatory disease of the conditional allele does not require presence of wild-type allele
|
|
• mice have pronounced leukocytic infiltrates in skin, liver, spleen, joint, sinus, conjunctiva, bone marrow, and tongue that are mainly neutrophilic
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
• neutrophils exhibit an unusual hypermature morphology characterized by nuclear hypersegmentation and blebbing
|
|
|
• neutrophil numbers are normal in these mice unlike the increased numbers observed in Mirn223tm1Fcam homozygotes
|
|
|
• neutorphils are hypersensitive to activating stimuli
• neutrophils have higher oxidative burst than controls upon low-dose PMA stimulation
• neutrophils display higher killing when co-cultured with Candida albicans
|
|
|
• neutrophils exhibit an unusual hypermature morphology characterized by nuclear hypersegmentation and blebbing
|
|
|
• neutrophil numbers are normal in these mice unlike the increased numbers observed in Mirn223tm1Fcam homozygotes
|
|
|
• neutorphils are hypersensitive to activating stimuli
• neutrophils have higher oxidative burst than controls upon low-dose PMA stimulation
• neutrophils display higher killing when co-cultured with Candida albicans
|
|
|
• neutrophils exhibit an unusual hypermature morphology characterized by nuclear hypersegmentation and blebbing
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• only 6.2% of bone marrow derived macrophages express MHC-II on the surface compared to 30% of controls
• incubation with IFN-gamma increases percentage to 19% which is much less than 72% of wild-type macrophages
|
|
• only 6.2% of bone marrow derived macrophages express MHC-II on the surface compared to 30% of controls
• incubation with IFN-gamma increases percentage to 19% which is much less than 72% of wild-type macrophages
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• during the early and middle phases of wound healing, mice exhibit reduced formation and vascularization of granulation tissue compared with control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• normal numbers of peritoneal macrophage
• no CTP:phosphocholine cytidylyltransferase alpha produced
• CTP:phosphocholine cytidylyltransferase, beta isoform upregulated
• severely reduced conversion of free cholesterol to phosphatidylcholine
• increased free cholesterol load leads to macrophage cell death
|
|
• normal numbers of peritoneal macrophage
• no CTP:phosphocholine cytidylyltransferase alpha produced
• CTP:phosphocholine cytidylyltransferase, beta isoform upregulated
• severely reduced conversion of free cholesterol to phosphatidylcholine
• increased free cholesterol load leads to macrophage cell death
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• normal myeloid lineage and in vitro M1 and M2 macrophage differentiation
|
|
• decrease in autophagosome formation in response to lipopolysaccharide injection or bacterial infection
|
|
• with TLR stimulation and pan-caspase inhibition treatments
|
|
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
|
|
• decrease in autophagosome formation in response to lipopolysaccharide injection or bacterial infection
|
|
• with TLR stimulation and pan-caspase inhibition treatments
|
|
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
|
|
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
|
|
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
|
|
• in cultured macrophages stimulated with LPS and ATP
|
|
• in cultured macrophages stimulated with LPS and ATP
|
|
• along with massive lung tissue destruction upon lipopoysaccharide injection
|
|
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
|
|
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
|
|
• with TLR stimulation and pan-caspase inhibition treatments
|
|
• higher in vitro macrophage cell death after lipopolysaccharide injection
|
|
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• increase in mortality after injection with high dose LPS (30 mg/kg)
|
|
• increased weight loss, higher colitis scores, and shorter colonic lengths following DSS induced colitis
|
|
• primary peritoneal macrophages show higher TNF-alpha and IL6 expression and secretion following stimulation with LPS, PGN, or poly(I:C)
|
|
• 4h after LPS stimulation
|
|
• 4h after LPS stimulation
|
|
• increase in infiltration of immune cells and more severe injuries after LPS treatment
|
|
• increase in mortality after injection with high dose LPS (30 mg/kg)
|
|
• increased weight loss, higher colitis scores, and shorter colonic lengths following DSS induced colitis
|
|
• 4h after LPS stimulation
|
|
• 4h after LPS stimulation
|
|
• primary peritoneal macrophages show higher TNF-alpha and IL6 expression and secretion following stimulation with LPS, PGN, or poly(I:C)
|
|
• increase in infiltration of immune cells and more severe injuries after LPS treatment
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice infected with HSV-1 exhibit increased mortality compared to controls
|
| N |
• mice show similar frequencies of F4/80+CD11b+ macrophages, natural killer cells, B cells, T cells, neutrophils, and monocytes in the spleen as in wild-type mice
|
|
• peritoneal macrophages infected with vaccinia virus (VACV) induces IFNB1 production to a certain level after 4 hours but shows no subsequent increases as seen in wild-type peritoneal macrophages
• macrophages infected with vaccinia virus show lower and less sustained IFNB1 expression than wild-type macrophages
|
|
• HSV-1 challenged mice exhibit severely attenuated serum IFN-beta concentrations
• however, serum IL-6, IFN-beta, and TNF-alpha concentrations are similar to wild-type mice after RNA virus Sendai virus infection
|
|
• HSV-1 infected peritoneal macrophages show decreased secretion of IFN-beta
|
|
• mice infected with herpes simplex type 1 virus (HSV-1)
|
|
• mice infected with HSV-1 exhibit increased mortality compared to controls
|
|
• peritoneal macrophages infected with vaccinia virus (VACV) induces IFNB1 production to a certain level after 4 hours but shows no subsequent increases as seen in wild-type peritoneal macrophages
• macrophages infected with vaccinia virus show lower and less sustained IFNB1 expression than wild-type macrophages
|
|
• HSV-1 challenged mice exhibit severely attenuated serum IFN-beta concentrations
• however, serum IL-6, IFN-beta, and TNF-alpha concentrations are similar to wild-type mice after RNA virus Sendai virus infection
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice do not develop lupus-like disease and do not exhibit an increase in anti-double stranded DNA antibodies or in anti-nuclear antibodies, do not show glomerular immune complex deposition, show normal serum creatinine levels and cytokine levels, and normal clearance of engulfed, dying cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice appear normal at weaning but fail to gain weight
|
|
• increase in levels of circulating neutrophils
|
|
• increase in levels of circulating lymphocytes
|
|
• increase in levels of circulating monocytes
|
|
• spleens show increased expression of interferon signature genes such as Ddx58 and Isg95
|
|
• IgG deposition in the glomeruli of kidneys
|
|
• macrophages exhibit an acute elevation of proinflammatory cytokines IL-1beta, IL-6, and IP-10, but not IL-10, in response to ingesting dying cells that is not seen in control macrophages
• however, neither bone marrow-derived macrophages nor peritoneal exudate macrophages from 52 week old mice show any defects in the engulfment of dying cells in vitro indicating normal phagocytic capacity
|
|
• levels of CXCL1, CCL4 and CCL2 are increased in 52-week old mice
|
|
• in 52-week old mice
|
|
• in 52-week old mice
|
|
• in 52-week old mice
|
|
• in 52-week old mice
|
|
• increase in levels of circulating neutrophils
|
|
• increase in levels of circulating lymphocytes
|
|
• increase in levels of circulating monocytes
|
|
• spleens show increased expression of interferon signature genes such as Ddx58 and Isg95
|
|
• IgG deposition in the glomeruli of kidneys
|
|
• macrophages exhibit an acute elevation of proinflammatory cytokines IL-1beta, IL-6, and IP-10, but not IL-10, in response to ingesting dying cells that is not seen in control macrophages
• however, neither bone marrow-derived macrophages nor peritoneal exudate macrophages from 52 week old mice show any defects in the engulfment of dying cells in vitro indicating normal phagocytic capacity
|
|
• levels of CXCL1, CCL4 and CCL2 are increased in 52-week old mice
|
|
• in 52-week old mice
|
|
• in 52-week old mice
|
|
• in 52-week old mice
|
|
• in 52-week old mice
|
|
• mice develop a systemic lupus erythematosus-like disease (SLE)
|
|
• increase in serum levels of a broad array of antibodies against autoantigens commonly associated with SLE
|
|
• kidneys from aged mice show endocapillary proliferative glomerulonephritis
|
|
• mice show indications of kidney damage and show increased functional markers of kidney injury
|
|
• IgG and complement C1q deposition in the glomeruli of kidneys
|
|
• kidneys from aged mice show endocapillary proliferative glomerulonephritis
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| systemic lupus erythematosus | DOID:9074 |
OMIM:152700 OMIM:300809 OMIM:605480 OMIM:608437 OMIM:609903 OMIM:609939 OMIM:610065 OMIM:610066 OMIM:612254 OMIM:612378 OMIM:613145 OMIM:614420 |
J:235399 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• increased migration into CNS in myelin oligodendrocyte glycoprotein MOG-CFA-induced EAE experiments
|
|
• significantly increased ROS production from CNS-infiltrating leukocytes in MOG-CFA-induced EAE experiments
• significantly increased malondialdehyde levels in CNS tissue in MOG-CFA-induced EAE experiments
|
|
• increased migration into CNS in myelin oligodendrocyte glycoprotein MOG-CFA-induced EAE experiments
|
|
• increased migration into CNS in myelin oligodendrocyte glycoprotein MOG-CFA-induced EAE experiments
|
|
• increased disease severity (lesions in central nervous system (CNS)) and high mortality in myelin oligodendrocyte glycoprotein (MOG)35-55-complete Freunds adjuvant (CFA)-induced EAE experiments
• when treated with reactive oxygen species (ROS) scavengers after EAE induction with MOG-CFA
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• tamoxifen treated mice do not develop arteriovenous malformations in response to AAV-VEGF injection into the basal ganglia at 8-10 weeks of age or around the ear tag wound
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• TNF levels in the serum of mice expressing Cre are lower by more than two thirds compared to controls 3 hours after LPS injection
|
|
• LPS stimulated release of TNF from macrophages is strongly reduced in these mice
|
|
• TNF levels in the serum of mice expressing Cre are lower by more than two thirds compared to controls 3 hours after LPS injection
|
|
• two weeks after induction of Cre recombinase, mice are more resistant to endotoxin shock than in controls
• 10 of 13 mice survive endotoxin induction with LPS and D-galactosamine while 11 of 13 controls die within 8 hours of injection
|
|
• LPS stimulated release of TNF from macrophages is strongly reduced in these mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• to the inflamed endothelium
|
|
• during TNF-alpha-induced inflammation, mice exhibit increased rolling influx, reduced percentage of crawling cells among adherent neutrophils and reduced number of adherent neutrophils to the inflamed endothelium
• neutrophils exhibit reduced neutrophil adhesion to ICAM-1-coated surface compared with wild-type cells
|
|
• to the inflamed endothelium
|
|
• during TNF-alpha-induced inflammation, mice exhibit increased rolling influx, reduced percentage of crawling cells among adherent neutrophils and reduced number of adherent neutrophils to the inflamed endothelium
• neutrophils exhibit reduced neutrophil adhesion to ICAM-1-coated surface compared with wild-type cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice fed standard chow or a high fat diet exhibit normal body weight and composition
|
| N |
• mice fed standard chow or a high fat diet exhibit normal glucose tolerance
|
| N |
• brown adipose tissue exhibits normal mitochondrial function (measured by cox activity)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• bone marrow derived macrophage show increased levels of LPS induced IL-10 mRNA and no further effect from addition PGE2 stimulation
|
|
• bone marrow derived macrophage show increased levels of LPS induced IL-10 mRNA and no further effect from addition PGE2 stimulation
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal perinatal survival
|
| N |
• mice exhibit normal lymphatic vessels with normal integrity
|
| N |
• mice do not exhibit edema
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• display increased bacterial titers in the blood and feces
• despite this mice survive the infection
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 50% mortality before 32 weeks of age
• mortality increases to 80% by 3-5 weeks if Lyz2tm1(cre)Ifo is homozygous
|
|
• 50% reduction in body size
|
|
• splenomegaly with loss of lymphoid follicles
• normal cell number but composition includes more large immature and myeloid cells and fewer lymphocytes
|
|
• increased number of neutrophiles
• decrease in thymocytes
|
|
• loss of a distinct medulla and cortex
|
|
• reduced bone marrow erythropoiesis
|
|
• splenic extramedullary myelopoiesis
|
|
• expanded number of neutrophiles
• reduced erythropoiesis
|
|
• thrombocytosis
|
|
• decreased percentage but not in absolute numbers in peripheral blood
• absolute number of B cells reduced in the spleen
|
|
• decreased percentage but not in absolute numbers in peripheral blood
|
|
• decreased percentage in peripheral blood
|
|
• slightly increased in absolute numbers in peripheral blood
|
|
• reduced numbers in the peritoneal cavity
|
|
• 5 fold increase in leukocytes in peripheral blood
|
|
• increased more than 10 fold
• accumulate in the lung alveolar spaces and around the large blood vessels
• accumulate in the small intestine, particularly the jejunum
• increased numbers in the peritoneal cavity
|
|
• increased more than 10 fold
• increase of the inflammatory subclass
|
|
• disrupted architecture
• granulocyte infiltration
• infiltration of neutrophiles
|
|
• splenomegaly with loss of lymphoid follicles
• normal cell number but composition includes more large immature and myeloid cells and fewer lymphocytes
|
|
• reduction in macrophage number
|
|
• loss of lymphoid follicles
|
|
• reduction in macrophage number
|
|
• increased number of neutrophiles
• decrease in thymocytes
|
|
• loss of a distinct medulla and cortex
|
|
• splenic extramedullary myelopoiesis
|
|
• decreased percentage but not in absolute numbers in peripheral blood
• absolute number of B cells reduced in the spleen
|
|
• decreased percentage but not in absolute numbers in peripheral blood
|
|
• decreased percentage in peripheral blood
|
|
• slightly increased in absolute numbers in peripheral blood
|
|
• reduced numbers in the peritoneal cavity
|
|
• 5 fold increase in leukocytes in peripheral blood
|
|
• increased more than 10 fold
• accumulate in the lung alveolar spaces and around the large blood vessels
• accumulate in the small intestine, particularly the jejunum
• increased numbers in the peritoneal cavity
|
|
• increased more than 10 fold
• increase of the inflammatory subclass
|
|
• disrupted architecture
• granulocyte infiltration
• infiltration of neutrophiles
|
|
• splenomegaly with loss of lymphoid follicles
• normal cell number but composition includes more large immature and myeloid cells and fewer lymphocytes
|
|
• reduction in macrophage number
|
|
• loss of lymphoid follicles
|
|
• reduction in macrophage number
|
|
• loss of lymphoid follicles
• infiltration of neutrophiles
• 4fewer macrophage
|
|
• increased number of neutrophiles
• decrease in thymocytes
|
|
• loss of a distinct medulla and cortex
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells
|
|
• macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells
• bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice
• macrophages lack homotypic adhesion unlike wild-type cells
|
|
• macrophage capacity to invade matrigel is severely defective compared with wild-type mice
• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells
• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
|
|
• in LPS-treated macrophages
|
|
• TPA-treated ears exhibit reduced inflammatory infiltration and edema compared with similarly treated wild-type cells
• following disruption of barrier function with 5% SDS (chronic cutaneous inflammation), mice fail to exhibit an inflammatory response as in similarly treated wild-type mice
|
|
• following oxygen-induced retinopathy, mice exhibit decreased repair of retinal damage compared with similarly treated wild-type mice
• CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells
|
|
• macrophage capacity to invade matrigel is severely defective compared with wild-type mice
• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells
• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
|
|
• CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells
|
|
• macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells
• bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice
• macrophages lack homotypic adhesion unlike wild-type cells
|
|
• macrophage capacity to invade matrigel is severely defective compared with wild-type mice
• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells
• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in LPS-treated mice compared with similarly treated wild-type mice
|
|
• 4 hours after LPS treatment
|
|
• 4 hours after LPS treatment
|
|
• 4 hours after LPS treatment
|
|
• 1.5 hrs after LPS treatment
|
|
• 1.5 and 4 hrs after LPS treatment
|
|
• LPS-treated mice exhibit less hypothermia, hypotension, and mortality; improved hemodynamic parameter, shock index, and heart rate to systolic blood pressure; and decreased macrophage cytokine production (TNF-alpha, IL6, IL12, IL1a, and IL1b) compared with similarly treated wild-type mice
|
|
• LPS-treated mice develop less hypothermia compared with similarly treated wild-type mice
|
|
• in LPS-treated mice compared with similarly treated wild-type mice
|
|
• LPS-treated mice develop less hypotension compared with similarly treated wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• tissue glucocerebrosidase activity is reduced to ~30-50% of control levels in all tissues
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice show normal weight gain at 10 weeks of age
|
|
• slight increase in IFN-gamma levels
|
|
• slight increase in IL-6 levels
|
|
• slight increase in TNF levels
|
| N |
• mice show no joint inflammation at 10 weeks of age, cytokine levels (such as IL-1 alpha, IL-1 beta, and MCP-1) are severely reduced, and the autoinflammatory disease seen in Gt(ROSA)26Sortm1(OVAL/fla-GFP)Vnce and Lyz2tm1(cre)Ifo expressing mice is almost entirely ameliorated
|
|
• slight increase in IFN-gamma levels
|
|
• slight increase in IL-6 levels
|
|
• slight increase in TNF levels
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal Th1 responses and do not develop colitis, unlike Stat3 null mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• an increased frequency of granulocyte-monocyte progenitors in the bone marrow
|
|
• bone marrow cells demonstrate a significant increase in both mature myeloid, immature myeloid and monocytic cells
|
|
• a decreased frequency of megakaryocyte-erythroid progenitors
|
|
• a decreased frequency of megakaryocyte-erythroid progenitors
|
|
• show a 2-fold increase in the numbers of circulating monocytes at 5 to 7 months of age
|
|
• bone marrow cells demonstrate a significant increase in both mature myeloid, immature myeloid and monocytic cells
|
|
• show a 2-fold increase in the numbers of circulating monocytes at 5 to 7 months of age
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in ovariectomized mice treated with 17beta-estradiol due to reduced re-epithelialization of the wound
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• S. aureus-infected mice exhibit an increased in viable S. aureus compared to in similarly treated wild-type mice
|
|
• S. aureus-infected mice exhibit an increased in viable S. aureus compared to in similarly treated wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• migration of neutrophils to the cite of bacterial infection is enhanced compared to in similarly treated wild-type mice
|
|
• S. aureus-infected mice exhibit a 3- to 4-fold increased in viable S. aureus compared to in similarly treated wild-type mice
|
|
• migration of neutrophils to the cite of bacterial infection is enhanced compared to in similarly treated wild-type mice
|
|
• S. aureus-infected mice exhibit a 3- to 4-fold increased in viable S. aureus compared to in similarly treated wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• osteoclasts exhibit decreased fusion during differentiation
|
|
• decreased size of multinucleate osteoclasts as compared to controls
• osteoclasts exhibit decreased fusion during differentiation
|
|
• osteoclasts exhibit decreased fusion during differentiation
|
|
• numbers of osteoclasts are decreased during differentiation
|
|
• decreased levels of serum type I collagen as compared to wild type
|
|
• decreased size of multinucleate osteoclasts as compared to controls
• osteoclasts exhibit decreased fusion during differentiation
|
|
• osteoclasts exhibit decreased fusion during differentiation
|
|
• numbers of osteoclasts are decreased during differentiation
|
|
• osteoclasts exhibit decreased fusion during differentiation
• decreased size of multinucleate osteoclasts as compared to controls
|
|
• osteoclasts exhibit decreased fusion during differentiation
|
|
• numbers of osteoclasts are decreased during differentiation
|
|
• increased bone mineral density is found in 2 and 6 month old mice as compared to controls
|
|
• increased trabecular bone volume in femoral and tibial bones
|
|
• macrophage infiltration is decreased in implanted subcutaneous tumors as compared to tumor implanted controls
|
|
• implanted melanoma cells have an increased live cell mass and volume as compared to tumor implanted controls
|
|
|
Analysis Tools