Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation
(9 available);
any
Cd86 mutation
(38 available)
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hematopoietic system
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• T cells primed to myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide exhibit modestly reduced proliferative responses as compared to than controls
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immune system
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• T cells primed to myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide exhibit modestly reduced proliferative responses as compared to than controls
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• lymph node cells from mice immunized with myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide produce more interferon gamma than wild type cells
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cellular
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• T cells primed to myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide exhibit modestly reduced proliferative responses as compared to than controls
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation
(9 available);
any
Cd86 mutation
(38 available)
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immune system
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• there is an absence of germinal center formation in mutants
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• when immunized with trinitrophenyl conjugates of keyhole limpet hemocyanin or ovalbumin, mice produce reduced levels of antibodies compared to wild-type
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• mice produce less than 5% of wild-type levels of IgG1 and IgG2a when immunized with keyhole limpet hemocyanin or ovalbumin conjugates
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hematopoietic system
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• there is an absence of germinal center formation in mutants
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• mice produce less than 5% of wild-type levels of IgG1 and IgG2a when immunized with keyhole limpet hemocyanin or ovalbumin conjugates
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation
(9 available);
any
Cd86 mutation
(38 available)
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behavior/neurological
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• forelimb grip strength starts weakening at 6 months of age and is less than half that of controls at 8 months of age
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• Background Sensitivity: by 20 weeks of age mice start to display a symmetrical mild hind leg paralysis that progresses to a generalized limb paralysis; by 32 weeks of age all female and 30% of male mutant mice display this with the majority of affected mice showing difficulty in walking; this phenotype is not seen when Cd86 nulls are crossed to C57BL/6 or 129/Sv nonautoimmune backgrounds
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• severe parapesis occurs to all mice by 28 weeks of age
• sciatic nerve conduction studies reveal a significant difference in distal latency, conduction velocity and amplitude of the motor response
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immune system
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• T cells proliferate in response to the auto-antigen myelin protein zero
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• transplanted diabetogenic T cells from Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi mice divided primarily in the pancreatic lymph nodes of NOD mice whereas, transferred T cells show reduced proliferation in Cd86-deficient NOD mice
• depletion of Tregs in Cd86-deficient mice partially restores proliferation of Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi T cells in pancreatic lymph nodes
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• in Cd86-deficient mice, numbers of regulatory T cells (Tregs) ie. CD4+CD25+Cd62Lhi, are reduced slightly in the spleen compared to control NOD mice
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• at 6 months of age, there is a 1.5 fold increase in the number of CD4+ T cells secreting IFN-gamma
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• no female or male mutants on the NOD background developed diabetes compared to 70% and 30% respectively in wild-type Cd86 NOD mice
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• when CD80 expression is blocked, 2-4-week old mice become diabetic, with 90% developing diabetes by 18 weeks; untreated mice are protected from diabetes
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• auto-antibodies to myelin protein zero are detected in sera of mice starting at 2-4 months of age
• by 8 months of age, all mice have detectable antibodies to this protein
• the isotype frequency are IgG3 > IgG1 > IgG2c > IgG2b
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nervous system
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• nulls display severe inflammation in the peripheral nervous system
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• some sciatic nerve fibers display increased numbers of Nodes of Ranvier with irregular spacing and irregular myelin sheet thickness
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• mice show mononuclear, cellular infiltrate composed of dendritic cells and scattered CD4+ and CD8+ cells
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• mice show mononuclear infiltrate in this structure
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• mice show mononuclear infiltrate in this structure
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• sciatic nerves show electrophysiological indications of a predominantly demyelinating neuropathy
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• a dipersion of compound muscle action potentials is observed
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• in the sciatic nerve, prolongation of distal latencies and a slowing of conduction velocity is seen with respect to wild-type NOD mice, with conduction block observed in severe cases
(J:71352)
• sciatic nerve conduction studies reveal a significant difference in distal latency, conduction velocity and amplitude of the motor response
(J:142046)
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• sciatic nerve conduction studies reveal a significant difference in conduction velocity
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muscle
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• skeletal muscles show severe focal neurogenic atrophy in severely affected animals, but there are no detectable lesions in the brain or spinal cord
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hematopoietic system
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• T cells proliferate in response to the auto-antigen myelin protein zero
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• transplanted diabetogenic T cells from Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi mice divided primarily in the pancreatic lymph nodes of NOD mice whereas, transferred T cells show reduced proliferation in Cd86-deficient NOD mice
• depletion of Tregs in Cd86-deficient mice partially restores proliferation of Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi T cells in pancreatic lymph nodes
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• in Cd86-deficient mice, numbers of regulatory T cells (Tregs) ie. CD4+CD25+Cd62Lhi, are reduced slightly in the spleen compared to control NOD mice
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cellular
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• T cells proliferate in response to the auto-antigen myelin protein zero
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• transplanted diabetogenic T cells from Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi mice divided primarily in the pancreatic lymph nodes of NOD mice whereas, transferred T cells show reduced proliferation in Cd86-deficient NOD mice
• depletion of Tregs in Cd86-deficient mice partially restores proliferation of Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi T cells in pancreatic lymph nodes
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hematopoietic system
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• T cells primed by MOG 355-55 peptide exhibit markedly impaired proliferative responses as compared to controls
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immune system
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• T cells primed by MOG 355-55 peptide exhibit markedly impaired proliferative responses as compared to controls
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• lymph node cells from mice immunized with MOG 355-55 peptide produce a greater than 30 fold increase in interferon gamma as compared to wild type cells
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• lymph node cells from mice immunized with MOG 355-55 peptide produce increased amounts of TNFalpha as compared to wild type cells, although the increase is limited to the first 24 hours of culture
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• mice do not develop clinical symptoms of EAE following stimulation by myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide or by adoptive transfer
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• 50% of mice exhibit inflammatory lesions in meninges and CNS parenchyma as compared to 80% in wild-type following 35 day observation period after EAE induction
• inflammatory foci are limited to leptomeninges
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nervous system
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• 50% of mice exhibit inflammatory lesions in meninges and CNS parenchyma as compared to 80% in wild-type following 35 day observation period after EAE induction
• inflammatory foci are limited to leptomeninges
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cellular
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• T cells primed by MOG 355-55 peptide exhibit markedly impaired proliferative responses as compared to controls
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immune system
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• in dendritic cells following LPS or anti-CD40 antibody stimulation
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• in dendritic cells following LPS or anti-CD40 antibody stimulation
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Analysis Tools