Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Unc93b13d mutation
(1 available);
any
Unc93b1 mutation
(38 available)
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immune system
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• disrupted TLR5-localization on plasma membrane of bone marrow-derived dendritic cells
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• DCs showed a moderate defect in an in vivo assay for T cell proliferation dependent on cross presentation by DCs
• splenic-derived dendritic cells do not secrete CD40 or CD86 upon flagellin stimulation
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• small intestine lamina propria dendritic cells do not secrete interleukin-12p40 upon flagellin stimulation
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• small intestine lamina propria-derived dendritic cells do not secrete interleukin-6 upon flagellin stimulation
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hematopoietic system
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• disrupted TLR5-localization on plasma membrane of bone marrow-derived dendritic cells
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Unc93b13d mutation
(1 available);
any
Unc93b1 mutation
(38 available)
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immune system
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• macrophages from homozygous mutant mice exhibit a "triple defect" in response to nucleic acids, failing to produce normal quantities of tumor necrosis factor (TNF) in response to poly(I)*poly(C), detected via TLR3; resiquimod, detected via TLR7; or oligonucleotides with unmethylated CpGs, detected via TLR9, although levels of all three TLRs in mutant whole-macrophage extracts are normal
• production of the costimulatory molecules CD40 and CD86 by peritoneal macrophages from homozygous mutants in response to each of the above inducers is significantly impaired; however, there is some response, though lower than in wild-type macrophages, to poly(I)*poly(C)
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• plasma levels of type I interferon 36 h after infection with mouse cytomegalovirus (MCMV) are greatly elevated in wild-type mice, but negligible in mutants
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• mutant dendritic cells exposed to apoptotic OVA-expressing cells or to OVA in solution fail to present OVA peptide in the context of H2-Kb
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• splenocytes harvested from homozygous mutant mice a week after their immunization with irradiated, ovallbumin- (OVA-) expressing C57BL/6 splenocytes and restimulated in vitro with an MHC class I-specific OVA peptide include no CD8+ IFNG+ cells recognizing the OVA peptide and exhibit no cytolytic activity against OVA peptide-bearing targets, demonstrating defective cross-presentation of antigen for MHC class I activation
• mutant dendritic cells exposed to apoptotic OVA-expressing cells or to OVA in solution fail to present OVA peptide in the context of H2-Kb
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• labeled CD4+ C57BL/6 T cells specific for ovalbumin (OVA) (OT-II cells) injected into mutant versus wild-type mice that are subsequently challenged with OVA exhibit a diminished in vivo proliferative response, demonstrating significantly less effective MHC class II antigen presentation by mutant antigen presenting cells (APCs)
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• infection of macrophages by Listeria monocytogenes elicits higher production of interleukin 12B (IL-12B) by wild-type than by mutant macrophages; this difference is greatly magnified for the hly mutant of L. monocytogenes, which cannot exit the phagosome
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• macrophages from homozygous mutant mice fail to produce normal quantities of tumor necrosis factor (TNF) in response to nucleic acid analogs
• plasma levels of TNF 36 h after infection with mouse cytomegalovirus (MCMV) are greatly elevated in wild-type mice, but negligible in mutants
• the TNF-alpha response curve of mutant mice following S. aureus infection parallels that of wild-type controls, but is shifted toward much higher bacterial loads
• infection of macrophages by Listeria monocytogenes elicits higher production of TNF by wild-type than by mutant macrophages; this difference is greatly magnified for the hly mutant of L. monocytogenes, which cannot exit the phagosome
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• infection of macrophages by Listeria monocytogenes elicits higher production of interleukin 12B (IL-12B) and of tumor necrosis factor (TNF) by wild-type than by mutant macrophages; this difference is greatly magnified for the hly mutant of L. monocytogenes, which cannot exit the phagosome
• 2 days after intravenous inoculation with luminescent Staphylococcus aureus, wild-type mice exhibit approximately the same level of luminescence as on day 1, whereas mutant mice show significantly higher levels than wild-type on day 1 and approximatley 3.5-fold more on day 2 than on day 1
• the TNF-alpha response curve of mutant mice following S. aureus infection parallels that of wild-type controls, but is shifted toward much higher bacterial loads
• one of seven S. aureus infected wild-type mice died (85% survival), whereas 3 of seven mutant mice succumbed to the infection (57% survival)
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• all homozygous mutant mice infected with mouse cytomegalovirus (MCMV), to which wild-type C57BL/6 mice are resistant, die within 5 days
• viral titers in homogenates of mutant spleens are 4 orders of magnitude greater than in control C57BL/6 spleen homogenates and comparable to those in spleens of susceptible BALB/c mice
• plasma levels of tumor necrosis factor (TNF) and type I interferon 36 h post infection with mouse cytomegalovirus (MCMV) are greatly elevated in wild-type mice, but negligible in mutants
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homeostasis/metabolism
hematopoietic system
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• macrophages from homozygous mutant mice exhibit a "triple defect" in response to nucleic acids, failing to produce normal quantities of tumor necrosis factor (TNF) in response to poly(I)*poly(C), detected via TLR3; resiquimod, detected via TLR7; or oligonucleotides with unmethylated CpGs, detected via TLR9, although levels of all three TLRs in mutant whole-macrophage extracts are normal
• production of the costimulatory molecules CD40 and CD86 by peritoneal macrophages from homozygous mutants in response to each of the above inducers is significantly impaired; however, there is some response, though lower than in wild-type macrophages, to poly(I)*poly(C)
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Analysis Tools