Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd276tm1Mak mutation
(0 available);
any
Cd276 mutation
(24 available)
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immune system
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• homozygotes develop more severe T helper 1 (TH1)-mediated lung inflammation than wild-type controls
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• homozygotes sensitized in TH1 conditions show a 6-fold increase of IFN-gamma levels in BAL fluid relative to wild-type controls
• when restimulated in vitro with OVA, pulmonary lymph node cell cultures derived from mutant mice sensitized in TH1 conditions produce ~3 times more IFN-gamma than wild-type cultures, indicating enhanced TH1 effector activity
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• upon OVA sensitization, homozygotes develop more severe airway inflammation than wild-type controls in T helper 1 (TH1) polarizing conditions (GM-CSF plus IL-12), as shown by a 3-fold increase in the number of activated (CD69+) CD4 and CD8 T cells in lung, a 6-fold rise in IFN-gamma levels in BAL fluid, and a 3-fold increase in IFN-gamma levels in pulmonary lymph node cell cultures from mice sensitized in TH1 conditions
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hematopoietic system
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• homozygotes develop more severe T helper 1 (TH1)-mediated lung inflammation than wild-type controls
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd276tm1Mak mutation
(0 available);
any
Cd276 mutation
(24 available)
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immune system
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N |
• following injection of lymphocytic choriomeningitis virus (LCMV) into the hind footpads, homozygotes show a normal CTL-mediated hypersensitivity reaction, with no differences in the extent and kinetics of footpad swelling relative to wild-type controls
• surprisingly, homozygotes display normal antiviral CTL responses to LCMV, influenza virus and vesicular stomatitis virus relative to wild-type controls
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• in MLR experiments, mutant irradiated B lymphoblasts (H-2b/b) show a 2-fold increase in their capacity to stimulate alloreactive T cells (both CD4 and CD8 populations) derived from BALB/c mice (H-2d/d) relative to wild-type B lymphoblasts
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• homozygotes develop more severe T helper 1 (TH1)-mediated lung inflammation than wild-type controls
• in contrast, TH2-mediated airway inflammation is similar to that in wild-type controls
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• homozygotes develop experimental autoimmune encephalomyelitis several days earlier than wild-type controls
• however, no differences in mean clinical scores are noted beyond day 20 and the rates of disease incidence are similar to those in wild-type controls
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• starting at ~17 months of age, homozygotes display significantly higher levels of serum autoantibodies to single-stranded DNA than wild-type controls
• however, spontaneous autoimmunity does not result in immune complex deposition in the glomeruli or lymphocytic infiltration into multiple organs
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• upon OVA sensitization, homozygotes develop more severe airway inflammation than wild-type controls in T helper 1 (TH1) polarizing conditions (GM-CSF plus IL-12), as shown by significantly increased total immune-inflammatory, lymphocyte and macrophage cell counts in the BAL fluid (2.7-fold) and lungs sections of mutant mice
• in contrast, OVA-sensitized homozygotes exhibit normal numbers of inflammatory cells in BAL and lung sections with no differences in eosinophilia or cytokine production by OVA-stimulated splenocytes relative to wild-type controls in TH2-polarizing conditions (GM-CSF alone), indicating that TH2-mediated lung inflammation is normal
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hematopoietic system
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• in MLR experiments, mutant irradiated B lymphoblasts (H-2b/b) show a 2-fold increase in their capacity to stimulate alloreactive T cells (both CD4 and CD8 populations) derived from BALB/c mice (H-2d/d) relative to wild-type B lymphoblasts
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• homozygotes develop more severe T helper 1 (TH1)-mediated lung inflammation than wild-type controls
• in contrast, TH2-mediated airway inflammation is similar to that in wild-type controls
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cellular
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• in MLR experiments, mutant irradiated B lymphoblasts (H-2b/b) show a 2-fold increase in their capacity to stimulate alloreactive T cells (both CD4 and CD8 populations) derived from BALB/c mice (H-2d/d) relative to wild-type B lymphoblasts
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Analysis Tools