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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cd86tm1Shr
targeted mutation 1, Arlene H Sharpe
MGI:1861805
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cd86tm1Shr/Cd86tm1Shr B6.129S4-Cd86tm1Shr MGI:5085306
hm2
Cd86tm1Shr/Cd86tm1Shr involves: 129S4/SvJae MGI:3618329
hm3
Cd86tm1Shr/Cd86tm1Shr NOD.129S4-Cd86tm1Shr MGI:3618096
cx4
Cd80tm1Shr/Cd80tm1Shr
Cd86tm1Shr/Cd86tm1Shr
B6.129S4-Cd80tm1Shr Cd86tm1Shr MGI:5085302
cx5
Cd86tm1Shr/Cd86tm1Shr
Marchf1tm1.1Sish/Marchf1tm1.1Sish
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4436871


Genotype
MGI:5085306
hm1
Allelic
Composition
Cd86tm1Shr/Cd86tm1Shr
Genetic
Background
B6.129S4-Cd86tm1Shr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation (9 available); any Cd86 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• T cells primed to myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide exhibit modestly reduced proliferative responses as compared to than controls

hematopoietic system
• T cells primed to myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide exhibit modestly reduced proliferative responses as compared to than controls

immune system
• T cells primed to myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide exhibit modestly reduced proliferative responses as compared to than controls
• lymph node cells from mice immunized with myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide produce more interferon gamma than wild type cells




Genotype
MGI:3618329
hm2
Allelic
Composition
Cd86tm1Shr/Cd86tm1Shr
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation (9 available); any Cd86 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• there is an absence of germinal center formation in mutants
• when immunized with trinitrophenyl conjugates of keyhole limpet hemocyanin or ovalbumin, mice produce reduced levels of antibodies compared to wild-type
• mice produce less than 5% of wild-type levels of IgG1 and IgG2a when immunized with keyhole limpet hemocyanin or ovalbumin conjugates

hematopoietic system
• there is an absence of germinal center formation in mutants
• mice produce less than 5% of wild-type levels of IgG1 and IgG2a when immunized with keyhole limpet hemocyanin or ovalbumin conjugates




Genotype
MGI:3618096
hm3
Allelic
Composition
Cd86tm1Shr/Cd86tm1Shr
Genetic
Background
NOD.129S4-Cd86tm1Shr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation (9 available); any Cd86 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• T cells proliferate in response to the auto-antigen myelin protein zero
• 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

behavior/neurological
• forelimb grip strength starts weakening at 6 months of age and is less than half that of controls at 8 months of age
• 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
• 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

immune system
• T cells proliferate in response to the auto-antigen myelin protein zero
• 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
• 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
• at 6 months of age, there is a 1.5 fold increase in the number of CD4+ T cells secreting IFN-gamma
• no female or male mutants on the NOD background developed diabetes compared to 70% and 30% respectively in wild-type Cd86 NOD mice
• 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
• 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

nervous system
• nulls display severe inflammation in the peripheral nervous system
• some sciatic nerve fibers display increased numbers of Nodes of Ranvier with irregular spacing and irregular myelin sheet thickness
• mice show mononuclear, cellular infiltrate composed of dendritic cells and scattered CD4+ and CD8+ cells
• mice show mononuclear infiltrate in this structure
• mice show mononuclear infiltrate in this structure
• sciatic nerves show electrophysiological indications of a predominantly demyelinating neuropathy
• a dipersion of compound muscle action potentials is observed
• 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)
• sciatic nerve conduction studies reveal a significant difference in conduction velocity

muscle
• skeletal muscles show severe focal neurogenic atrophy in severely affected animals, but there are no detectable lesions in the brain or spinal cord

hematopoietic system
• T cells proliferate in response to the auto-antigen myelin protein zero
• 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
• 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

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Guillain-Barre syndrome DOID:12842 OMIM:139393
J:71352 , J:142046




Genotype
MGI:5085302
cx4
Allelic
Composition
Cd80tm1Shr/Cd80tm1Shr
Cd86tm1Shr/Cd86tm1Shr
Genetic
Background
B6.129S4-Cd80tm1Shr Cd86tm1Shr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd80tm1Shr mutation (12 available); any Cd80 mutation (43 available)
Cd86tm1Shr mutation (9 available); any Cd86 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• T cells primed by MOG 355-55 peptide exhibit markedly impaired proliferative responses as compared to controls

hematopoietic system
• T cells primed by MOG 355-55 peptide exhibit markedly impaired proliferative responses as compared to controls

immune system
• T cells primed by MOG 355-55 peptide exhibit markedly impaired proliferative responses as compared to controls
• 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
• 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
• mice do not develop clinical symptoms of EAE following stimulation by myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide or by adoptive transfer
• 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

nervous system
• 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




Genotype
MGI:4436871
cx5
Allelic
Composition
Cd86tm1Shr/Cd86tm1Shr
Marchf1tm1.1Sish/Marchf1tm1.1Sish
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd86tm1Shr mutation (9 available); any Cd86 mutation (29 available)
Marchf1tm1.1Sish mutation (1 available); any Marchf1 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• in dendritic cells following LPS or anti-CD40 antibody stimulation
• in dendritic cells following LPS or anti-CD40 antibody stimulation





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
01/12/2022
MGI 6.17
The Jackson Laboratory