All Phenotypes Igh-J<tm1Aigl> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Igh-J^tm1Aigl
targeted mutation 1, Antonio Iglesias
MGI:3665428

Summary

5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Igh-J^tm1Aigl/Igh-J⁺	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3688084
ht2	Igh-J^tm1Aigl/Igh-J⁺	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3688085
cx3	Igh-J^tm1Aigl/Igh-J⁺ Mog^tm1Dpd/Mog^tm1Dpd Tg(Tcra2D2,Tcrb2D2)1Kuch/0	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:4461060
cx4	Igh-J^tm1Aigl/Igh-J⁺ Tg(Tcra2D2,Tcrb2D2)1Kuch/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:4461059
cx5	Igh-J^tm1Aigl/Igh-J^tm1Aigl Tg(H2-K^b-Tcra,-Tcrb)1640Kurs/0	involves: 129S1/Sv * 129X1/SvJ * FVB/N * SJL/J	MGI:5644519

Allelic Composition	Igh-J^tm1Aigl/Igh-J⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igh-J^tm1Aigl mutation (0 available); any Igh-J mutation (13 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

abnormal B cell morphology ( J:111543 )

• only a few (1-4%) of B cells express endogenous the endogenous IgH; almost all cells express transgenic IgM^a

• prior to MOG-immunization, ratio of replacement to substitution mutations (R/S) in B cell V region is much lower than 14 days after immunization; R/S ratio (R/S: 3.4) is 3-fold higher than in preimmune sequences (R/S 1.4) and for the compelementarity-determining region 3, R/S ratio is 14.5 on day 14 vs 1.5 at day 0

decreased B cell number ( J:111543 )

decreased B-1 B cell number ( J:111543 )

increased susceptibility to experimental autoimmune encephalomyelitis ( J:111543 )

• EAE induced with rMOG protein occurs in 70% of animals vs 29% in wild-type littermates; wild-type C57BL/6 mice are only partially susceptible to MOG-induced EAE

hematopoietic system

abnormal B cell morphology ( J:111543 )

• only a few (1-4%) of B cells express endogenous the endogenous IgH; almost all cells express transgenic IgM^a

decreased B cell number ( J:111543 )

decreased B-1 B cell number ( J:111543 )

Allelic Composition	Igh-J^tm1Aigl/Igh-J⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igh-J^tm1Aigl mutation (0 available); any Igh-J mutation (13 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

increased susceptibility to experimental autoimmune encephalomyelitis ( J:111543 )

• transgenic mice immunized with PLP peptide or rMOG protein show accelerated onset of experimental autoimmune encephalitis (EAE) and exacerbated the neurological deficit to a maximal disease score of 4.9 vs 2.1 in nontransgenic littermate controls

• with adoptive transfer of PLP peptide specific SJL T cell lines which induce severe, often lethal EAE, disease onset occurs 3-4 days earlier than in nontransgenic littermates

Allelic Composition	Igh-J^tm1Aigl/Igh-J⁺ Mog^tm1Dpd/Mog^tm1Dpd Tg(Tcra2D2,Tcrb2D2)1Kuch/0
Genetic Background	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igh-J^tm1Aigl mutation (0 available); any Igh-J mutation (13 available)
Mog^tm1Dpd mutation (0 available); any Mog mutation (58 available)
Tg(Tcra2D2,Tcrb2D2)1Kuch mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

paralysis ( J:151335 )

• disease started between 7 and 10 weeks of age, with classical paralytic EAE signs

muscle

muscle hypertonia ( J:151335 )

• in a minority of cases, with a spastic component

nervous system

CNS inflammation ( J:151335 )

• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues

abnormal nervous system morphology ( J:151335 )

• inflammatory infiltrates in the peripheral nervous system despite the absence of MOG within these tissues

abnormal optic nerve morphology ( J:151335 )

• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve

abnormal spinal cord morphology ( J:151335 )

• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in the spinal cord

demyelination ( J:151335 )

• within the spinal cord and optic nerve

vision/eye

abnormal optic nerve morphology ( J:151335 )

• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve

immune system

increased susceptibility to experimental autoimmune encephalomyelitis ( J:151335 )

• 15% of the mice develop spontaneous EAE

CNS inflammation ( J:151335 )

• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
multiple sclerosis		DOID:2377	OMIM:612594 OMIM:612595 OMIM:612596	J:151335

Allelic Composition	Igh-J^tm1Aigl/Igh-J⁺ Tg(Tcra2D2,Tcrb2D2)1Kuch/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igh-J^tm1Aigl mutation (0 available); any Igh-J mutation (13 available)
Tg(Tcra2D2,Tcrb2D2)1Kuch mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

paralysis ( J:151335 )

• disease started between 7 and 10 weeks of age, with classical paralytic EAE signs

immune system

increased susceptibility to experimental autoimmune encephalomyelitis ( J:151335 )

• fifty percent spontaneously develop opticospinal myelitis

CNS inflammation ( J:151335 )

• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues

muscle

muscle hypertonia ( J:151335 )

• in a minority of cases, with a spastic component

nervous system

CNS inflammation ( J:151335 )

• inflammatory infiltrates in the trigeminal ganglia, spinal ganglia, spinal roots despite the absence of MOG within these tissues

abnormal nervous system morphology ( J:151335 )

• inflammatory infiltrates in the peripheral nervous system despite the absence of MOG within these tissues

abnormal optic nerve morphology ( J:151335 )

• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve

abnormal spinal cord morphology ( J:151335 )

• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in the spinal cord

demyelination ( J:151335 )

• within the spinal cord and optic nerve

vision/eye

abnormal optic nerve morphology ( J:151335 )

• lesions consisting of lymphocytic infiltration, demyelation and axonal damage in optic nerve

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
multiple sclerosis		DOID:2377	OMIM:612594 OMIM:612595 OMIM:612596	J:151335

Allelic Composition	Igh-J^tm1Aigl/Igh-J^tm1Aigl Tg(H2-K^b-Tcra,-Tcrb)1640Kurs/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * FVB/N * SJL/J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igh-J^tm1Aigl mutation (0 available); any Igh-J mutation (13 available)
Tg(H2-K^b-Tcra,-Tcrb)1640Kurs mutation (0 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Ig deposition and B cell infiltrates in spinal cord of sick Tg(H2-K^b-Tcra,-Tcrb)1640Kurs/0 Igh-J^tm1Aigl/Igh-J^tm1Aigl and Tg(H2-K^b-Tcra,-Tcrb)1640Kurs/0 mice

immune system

increased susceptibility to experimental autoimmune encephalomyelitis ( J:149511 )

• mice develop spontaneous experimental autoimmune encephalomyelitis (EAE) at high frequency

• almost all females develop EAE by 120 days of age, while fewer than 40% develop EAE by this time

increased autoantibody level ( J:149511 )

• mice produce anti-MOG autoantibodies, dominated by the transgene specific allotype Igh^a

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