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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cd276tm1Mak
targeted mutation 1, Tak Mak
MGI:3033707
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cd276tm1Mak/Cd276tm1Mak C.129P2-Cd276tm1Mak MGI:3033860
hm2
Cd276tm1Mak/Cd276tm1Mak involves: 129P2/OlaHsd * C57BL/6 MGI:3033710


Genotype
MGI:3033860
hm1
Allelic
Composition
Cd276tm1Mak/Cd276tm1Mak
Genetic
Background
C.129P2-Cd276tm1Mak
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd276tm1Mak mutation (0 available); any Cd276 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• homozygotes develop more severe T helper 1 (TH1)-mediated lung inflammation than wild-type controls
• 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
• 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

hematopoietic system
• homozygotes develop more severe T helper 1 (TH1)-mediated lung inflammation than wild-type controls




Genotype
MGI:3033710
hm2
Allelic
Composition
Cd276tm1Mak/Cd276tm1Mak
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd276tm1Mak mutation (0 available); any Cd276 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
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
• 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
• 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
• 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
• 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
• 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

hematopoietic system
• 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
• 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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last database update
11/07/2017
MGI 6.11
The Jackson Laboratory