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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ighmtm1Cgn
targeted mutation 1, University of Cologne
MGI:1857187
Summary 32 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ighmtm1Cgn/Ighmtm1Cgn B6.129S2-Ighmtm1Cgn MGI:3767416
hm2
Ighmtm1Cgn/Ighmtm1Cgn B6.129S2-Ighmtm1Cgn/J MGI:3700262
hm3
Ighmtm1Cgn/Ighmtm1Cgn involves: 129S2/SvPas MGI:3702915
hm4
Ighmtm1Cgn/Ighmtm1Cgn involves: 129S2/SvPas * C57BL/6 MGI:2179146
hm5
Ighmtm1Cgn/Ighmtm1Cgn NOD.129S2-Ighmtm1Cgn MGI:3623425
hm6
Ighmtm1Cgn/Ighmtm1Cgn NOD.129S2-Ighmtm1Cgn/DvsJ MGI:3793300
hm7
Ighmtm1Cgn/Ighmtm1Cgn NODCaj.129S2-Ighmtm1Cgn MGI:3623420
ht8
Ighmtm1Cgn/Ighm+ involves: 129S2/SvPas * C57BL/6 MGI:3767232
ht9
Ighmtm1Cgn/Ighm+ NOD.129S2-Ighmtm1Cgn MGI:3623426
cx10
Ighmtm1Cgn/Ighmtm1Cgn
X/Yaa
BXSB.129S2(B6)-Ighmtm1Cgn/Dcr MGI:6107168
cx11
Ighmtm1Cgn/Ighmtm1Cgn
Igkctm1Bgmn/Igkctm1Bgmn
Igltm2.1Bgmn/Igltm2.1Bgmn
involves: 129 MGI:3806699
cx12
Ighmtm1Cgn/Ightm3Tim involves: 129 * C57BL/6 MGI:3610407
cx13
Ighmtm1Cgn/Ighmtm1Cgn
Trex1tm1Tld/Trex1tm1Tld
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:5317333
cx14
Ighmtm1Cgn/Ighmtm1Cgn
Unc93b1tm1.1Kmiy/Unc93b1tm1.1Kmiy
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:5140974
cx15
Faslgld/Faslgld
Ighmtm1Cgn/Ighmtm1Cgn
involves: 129S2/SvPas * C3H/HeJ * C57BL/6 MGI:3767450
cx16
Ighmtm1Cgn/Ighmtm1Cgn
Nlrp1aNeut1/Nlrp1aNeut1
involves: 129S2/SvPas * C57BL/6 MGI:5474290
cx17
Ighmtm1Cgn/Ighmtm1Cgn
Irf2tm1Mak/Irf2tm1Mak
involves: 129S2/SvPas * C57BL/6 MGI:3630271
cx18
Ighmtm1Cgn/Ighmtm1Cgn
Tgfb1tm1Doe/Tgfb1tm1Doe
involves: 129S2/SvPas * C57BL/6 * CF-1 MGI:3622465
cx19
Ighmtm1Cgn/Ighm+
Tgfb1tm1Doe/Tgfb1tm1Doe
involves: 129S2/SvPas * C57BL/6 * CF-1 MGI:3622466
cx20
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Ins2-Cxcl13)1Cys/0
involves: 129S2/SvPas * C57BL/6 * DBA/2 MGI:3689372
cx21
Faslpr/Faslpr
Ighmtm1Cgn/Ighmtm1Cgn
involves: 129S2/SvPas * C57BL/6 * MRL/Mp MGI:3767451
cx22
Ighmtm1Cgn/Ighmtm1Cgn
Tg(TcraR28,TcrbR28)KRNDim/0
involves: 129S2/SvPas * C57BL/6 * NOD * SJL MGI:3842821
cx23
Ighmtm1Cgn/Ighmtm1Cgn
Tg(IghMyc)22Bri/0
involves: 129S2/SvPas * C57BL * SJL MGI:5437736
cx24
Ighmtm1Cgn/Ighmtm1Cgn
Ptpn6me-v/Ptpn6me-v
involves: 129S7/SvEvBrd * C57BL/6J MGI:6383231
cx25
Ighmtm1Cgn/Ighmtm1Cgn
Tnftm2Gkl/Tnf+
involves: 129S/SvEv * 129S2/SvPas * C57BL/6J MGI:3629519
cx26
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Igh-VB1-8/Igh-6m)1Mjsk/?
NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ MGI:3581965
cx27
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Ighmtm1Cgn/Ighmtm1Cgn
Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell
NOD.Cg-Ighmtm1Cgn H2-Ab1b-tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell MGI:3687129
cx28
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Igh-6/Igh-V125)2Jwt/0
Tg(Igk-C/Igk-V125)1Jwt/0
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V125)2Jwt Tg(Igk-C/Igk-V125)1Jwt MGI:3623595
cx29
Ighmtm1Cgn/Ighm+
Tg(Igh-6/Igh-V125)2Jwt/0
Tg(Igk-C/Igk-V125)1Jwt/0
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V125)2Jwt Tg(Igk-C/Igk-V125)1Jwt MGI:3623596
cx30
Ighmtm1Cgn/Ighm+
Tg(Igh-6/Igh-V281)3Jwt/0
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V281)3Jwt MGI:3623593
cx31
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Igh-6/Igh-V281)3Jwt/0
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V281)3Jwt MGI:3623592
cx32
Ighmtm1Cgn/Ighmtm1Cgn
Tg(IghelMD4)4Ccg/Tg(IghelMD4)4Ccg
NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ MGI:3793299


Genotype
MGI:3767416
hm1
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
B6.129S2-Ighmtm1Cgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• migration of proliferated intestinal epithelial cells (IEC) toward the top of the villi and the number of proliferating IECs are augmented in mutants compared to wild-type controls
• treatment of mice with antibiotics results in deceleration of IEC migration and decreased proliferation compared to treated heterozygous controls

hematopoietic system
• population is ~2 times larger than in heterozygous controls

immune system
• population is ~2 times larger than in heterozygous controls




Genotype
MGI:3700262
hm2
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
B6.129S2-Ighmtm1Cgn/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• T cell numbers in lymph nodes are normal (J:73100)
• dendritic cells show normal function in mutants (J:118565)
• a transitional block in early B cell development in evident in bone marrow; pre-B cells are decreased in number
• numbers of CD11c+ dendritic cells (DCs) are reduced in mutants
• numbers are reduced 3-fold in spleen vs wild-type (J:73100)
• there are 5- to 40-fold fewer antigen specific CD4 cells producing Il-2 in mutants compared to controls 6 months after keyhole limpet hemocyanin immunization (J:118565)
• numbers are reduced 3-fold in spleen vs wild-type
• in mutants, area of T zone stromal cell network in the spleen is decreased four- to five-fold compared to wild-type
• T zone cross sectional area is decreased 2- to 3-fold
• spleens are ~50% the weight of wild-type spleens
• mice fail to respond to T cell-dependent (OVA) or T cell-independent (dextra) antigenic stimulation and do not produce serum specific antibodies to these antigens
• null mice have almost undetectable serum levels of IgG1, IgG2a, IgG2b, IgG3, IgM and IgA compared to wild-type controls or Faslpr mice
• IgE is not detectable in serum of OVA-treated mutants, but high levels are produced in treated wild-type
• IgG levels drop rapidly after birth due to loss of maternal Ig (J:119584)
• IgG is not detectable in OVA-treated mutants, but high levels are produced in treated wild-type (J:125656)
• IgG1 is not detected in serum after OVA challenge
• in mutants, Il-2 secretion is diminished from T cells primed in absence of B cells compared to controls 6 months after keyhole limpet hemocyanin immunization
• mice fail to clear a Giardia muris infection
• two weeks after Giardia infection, there are 10-fold more Giardia cysts present in the feces of mice
• mice have 10-fold more Giardia trophozoites in the small intestine three weeks after infection and a thousand-fold more 7 weeks after infection compared to controls
• mutant mice still have an active Giardia population in the gut one year after infection while wild-type mice clear Giardia after about 7 weeks
• mice are not protected from Giardia upon a secondary challenge as wild-type mice are

hematopoietic system
• a transitional block in early B cell development in evident in bone marrow; pre-B cells are decreased in number
• numbers of CD11c+ dendritic cells (DCs) are reduced in mutants
• numbers are reduced 3-fold in spleen vs wild-type (J:73100)
• there are 5- to 40-fold fewer antigen specific CD4 cells producing Il-2 in mutants compared to controls 6 months after keyhole limpet hemocyanin immunization (J:118565)
• numbers are reduced 3-fold in spleen vs wild-type
• in mutants, area of T zone stromal cell network in the spleen is decreased four- to five-fold compared to wild-type
• T zone cross sectional area is decreased 2- to 3-fold
• spleens are ~50% the weight of wild-type spleens
• null mice have almost undetectable serum levels of IgG1, IgG2a, IgG2b, IgG3, IgM and IgA compared to wild-type controls or Faslpr mice
• IgE is not detectable in serum of OVA-treated mutants, but high levels are produced in treated wild-type
• IgG levels drop rapidly after birth due to loss of maternal Ig (J:119584)
• IgG is not detectable in OVA-treated mutants, but high levels are produced in treated wild-type (J:125656)
• IgG1 is not detected in serum after OVA challenge

respiratory system
• ovalbumin-sensitized/challenged mice (OVA) are unable to generate an early phase reaction (EPR- initial phase of brochoconstriction) following OVA provocation

cardiovascular system
• mutants are protected from developing elastase-induced abdominal aortic aneurysm

homeostasis/metabolism
• mutants are protected from developing elastase-induced abdominal aortic aneurysm
• reconstitution of mutants with mouse natural antibodies from pooled sera of wild-type mice does not restore susceptibility to abdominal aortic aneurysm in mutants, however reconstitution with pooled mouse IgG to the wild-type level renders mutants susceptible to abdominal aortic aneurysm

skeleton
• significantly decreased at 10 weeks of age
• reduced trabecular bone structure in femora
• reduced number of trabeculae




Genotype
MGI:3702915
hm3
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• CD4+ T cells isolated from antigen-challenged mice have reduced proliferation in response to antigen encounter in vitro
• B cell development is halted at pre-B cell stage, indicated by lack of CD25+ B-cells
• in bone marrow and spleen, mature (B220+) B lymphocytes are lacking
• marginal metallophilic macrophages are absent
• sinus lining cells (MAdCAM-1+) are absent
• CD4+ T cells isolated from antigen-challenged mice have reduced proliferation in response to antigen encounter in vitro
• follicular dendritic cells are absent
• footpad swelling of antigen-sensitized mice is less than controls
• CD4+ T cells have normal primary responses suggesting lower T cell activity from immunized mice is a failure in antigen presentation
• after second infestation to ticks, mice fail to exhibit resistance (repletion) unlike similarly treated wild-type mice

hematopoietic system
• CD4+ T cells isolated from antigen-challenged mice have reduced proliferation in response to antigen encounter in vitro
• B cell development is halted at pre-B cell stage, indicated by lack of CD25+ B-cells
• in bone marrow and spleen, mature (B220+) B lymphocytes are lacking
• marginal metallophilic macrophages are absent
• sinus lining cells (MAdCAM-1+) are absent
• CD4+ T cells isolated from antigen-challenged mice have reduced proliferation in response to antigen encounter in vitro

skeleton

cellular
• CD4+ T cells isolated from antigen-challenged mice have reduced proliferation in response to antigen encounter in vitro




Genotype
MGI:2179146
hm4
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mucosal-associated invariant T cells (MAIT) that are not found in mice lacking all B cells are found in normal amounts in these mice
• mutants appear to have large pre-B cells, but not small pre-B cells, indicating arrest of differentiation at the pre-B cell stage at or close to the transition from the large to small pre-B cell (J:64298)
• in heterozygotes, normal numbers of B cells are produced, but there is loss of H-chain allelic exclusion; B cells producing H chains from both endogenous loci are detected, but such cells are absent in wild-type mice (J:70398)
• development appears to arrest differentiation of B cells at or close to the transition from the large to small pre-B cell
• no B cells are detected in the peritoneal cavity; no cells expressing IgM or IgD on their surface are detected in the peritoneal cavity
• peripheral blood and spleen lack mature B cells as shown by lack of CD45R(B220)bright cells
• homozygotes have no detectable IgM in their serum compared to ~600ug IgM/ml in wild-type serum
• upon infection with Mycoplasma pulmonis, airway lymphatic vessel remodeling is largely absent from mutants, compared to significant invasion of region by lymphatic vessels in infected wild-type mice
• bacteria are present in liver and kidney of mice after 4 weeks of M. pulmonis infection, but bacteria are absent from wild-type mouse tissue
• airway vascular and airway lymphatic vessel remodeling are impaired or absent compared to wild-type mice after M. pulmonis infection

hematopoietic system
• mutants appear to have large pre-B cells, but not small pre-B cells, indicating arrest of differentiation at the pre-B cell stage at or close to the transition from the large to small pre-B cell (J:64298)
• in heterozygotes, normal numbers of B cells are produced, but there is loss of H-chain allelic exclusion; B cells producing H chains from both endogenous loci are detected, but such cells are absent in wild-type mice (J:70398)
• development appears to arrest differentiation of B cells at or close to the transition from the large to small pre-B cell
• no B cells are detected in the peritoneal cavity; no cells expressing IgM or IgD on their surface are detected in the peritoneal cavity
• peripheral blood and spleen lack mature B cells as shown by lack of CD45R(B220)bright cells
• homozygotes have no detectable IgM in their serum compared to ~600ug IgM/ml in wild-type serum

respiratory system
N
• trachea of infected mice contain more mucin than infected wild-type tracheas
• after 4 weeks, mice show absence of vascular remodeling of the airways in response to Mycoplasma pulmonis infection wherease wild-type show complex growth and reorganization of the vascular beds
• although epithelial cell hyperplasia is not observed, epithelial layer is abnormally elongated




Genotype
MGI:3623425
hm5
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
NOD.129S2-Ighmtm1Cgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• no male or female homozygotes develop diabetes (assessed by glycosuric levels >3) by 20 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
NOT type 1 diabetes mellitus DOID:9744 OMIM:222100
J:37287




Genotype
MGI:3793300
hm6
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
NOD.129S2-Ighmtm1Cgn/DvsJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD

immune system
• T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD
• B cells are absent in the spleen
• the proportion, but not the number, of CD 4 and CD8 T cells found in the spleen is increased due to the absence of B cells
• follicles do not develop in the spleen
• 13.6% of female mice develop diabetes by 21 weeks of age compared to control NOD mice that have an incidence rate of 95.5% at this age

hematopoietic system
• T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD
• B cells are absent in the spleen
• the proportion, but not the number, of CD 4 and CD8 T cells found in the spleen is increased due to the absence of B cells
• follicles do not develop in the spleen

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
NOT type 1 diabetes mellitus DOID:9744 OMIM:222100
J:80859




Genotype
MGI:3623420
hm7
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
NODCaj.129S2-Ighmtm1Cgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice display insulitis starting at 8 weeks; insulitis is milder than that observed in NOD control mice

immune system
• mice display insulitis starting at 8 weeks; insulitis is milder than that observed in NOD control mice




Genotype
MGI:3767232
ht8
Allelic
Composition
Ighmtm1Cgn/Ighm+
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• B cell development is arrested at the stage of pre-B cells

immune system
• B cell development is arrested at the stage of pre-B cells




Genotype
MGI:3623426
ht9
Allelic
Composition
Ighmtm1Cgn/Ighm+
Genetic
Background
NOD.129S2-Ighmtm1Cgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• 90% of female and 45% of male heterozygotes develop diabetes (glycosuric values >3) by 20 weeks of age compared to 0% of homozygotes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:37287




Genotype
MGI:6107168
cx10
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
X/Yaa
Genetic
Background
BXSB.129S2(B6)-Ighmtm1Cgn/Dcr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Yaa mutation (24 available); any Yaa mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• this null allele diminishes the B cells essential for the Yaa-induced development of Lupus-like autoimmune disease such that these males survive beyond 40 weeks, and do not have the increased splenic populations of CD4+ T cells or CD11b+ monocytes, nor is there elevated ICOS expression in splenic T cells




Genotype
MGI:3806699
cx11
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Igkctm1Bgmn/Igkctm1Bgmn
Igltm2.1Bgmn/Igltm2.1Bgmn
Genetic
Background
involves: 129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Igkctm1Bgmn mutation (0 available); any Igkc mutation (9 available)
Igltm2.1Bgmn mutation (0 available); any Igl mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• IgG is not present in the sera
• IgM is not present in the sera

hematopoietic system
• IgG is not present in the sera
• IgM is not present in the sera




Genotype
MGI:3610407
cx12
Allelic
Composition
Ighmtm1Cgn/Ightm3Tim
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Ightm3Tim mutation (0 available); any Igh mutation (44 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• preferentially promoted development to marginal zone B cell
• inefficiently drives bone marrow B lymphopoiesis and follicular B cell development
• B cell in mutants are reduced in the spleen, bone marrow and LNs

immune system
• preferentially promoted development to marginal zone B cell
• inefficiently drives bone marrow B lymphopoiesis and follicular B cell development
• B cell in mutants are reduced in the spleen, bone marrow and LNs




Genotype
MGI:5317333
cx13
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Trex1tm1Tld/Trex1tm1Tld
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Trex1tm1Tld mutation (3 available); any Trex1 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• compared with Ighmtm1Cgn homozygotes
• however, the premature death observed in Trex1tm1Tld homozygotes is rescued

immune system
• as in Trex1tm1Tld homozygotes
• as in Trex1tm1Tld homozygotes
• as in Trex1tm1Tld homozygotes
• unlike in Trex1tm1Tld homozygotes

renal/urinary system
N
• unlike Trex1tm1Tld homozygotes, mice do not exhibit glomerular lesions
• as in Trex1tm1Tld homozygotes
• unlike in Trex1tm1Tld homozygotes

cardiovascular system
• as in Trex1tm1Tld homozygotes
• as in Trex1tm1Tld homozygotes




Genotype
MGI:5140974
cx14
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Unc93b1tm1.1Kmiy/Unc93b1tm1.1Kmiy
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Unc93b1tm1.1Kmiy mutation (6 available); any Unc93b1 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• unlike Unc93b1tm1.1Kmiy homozygotes, mice do not exhibit premature death

hematopoietic system
N
• unlike in Unc93b1tm1.1Kmiy homozygotes, spleen size is normal
• unlike in Unc93b1tm1.1Kmiy homozygotes, mice do not exhibit differentiation towards memory CD4+ T cells
• not as severe as in Unc93b1tm1.1Kmiy homozygotes




Genotype
MGI:3767450
cx15
Allelic
Composition
Faslgld/Faslgld
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
involves: 129S2/SvPas * C3H/HeJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Faslgld mutation (7 available); any Fasl mutation (37 available)
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice have high levels of IgG after birth that rise to levels similar to wild-type littermates by 90 days after birth




Genotype
MGI:5474290
cx16
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Nlrp1aNeut1/Nlrp1aNeut1
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Nlrp1aNeut1 mutation (0 available); any Nlrp1a mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• no abnormal neutrophil infiltration of the dermis




Genotype
MGI:3630271
cx17
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Irf2tm1Mak/Irf2tm1Mak
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Irf2tm1Mak mutation (1 available); any Irf2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• mice develop similar skin symptoms to Irf2-null mice




Genotype
MGI:3622465
cx18
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tgfb1tm1Doe/Tgfb1tm1Doe
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CF-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tgfb1tm1Doe mutation (4 available); any Tgfb1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive for a median of 35 days

growth/size/body
• mutants display a wasting syndrome which results in death 2-5 days after the start of weight loss

immune system
• animals display decreased thymic cellularity
• animals develop inflammation similar to that displayed by Tgfb1 nulls, although this is delayed by about 2 weeks

hematopoietic system
• animals display decreased thymic cellularity

endocrine/exocrine glands
• animals display decreased thymic cellularity




Genotype
MGI:3622466
cx19
Allelic
Composition
Ighmtm1Cgn/Ighm+
Tgfb1tm1Doe/Tgfb1tm1Doe
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CF-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tgfb1tm1Doe mutation (4 available); any Tgfb1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• splenocytes of Day 12-19 mutants are hyperresponsive to LPS stimulation in culture compared to Igh-6 heterozygous splenocytes

immune system
• animals display decreased thymic cellularity

hematopoietic system
• animals display decreased thymic cellularity

endocrine/exocrine glands
• animals display decreased thymic cellularity




Genotype
MGI:3689372
cx20
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Ins2-Cxcl13)1Cys/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(Ins2-Cxcl13)1Cys mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• very few infiltrates of pancreatic islets are observed
• infiltrates are B cell dominated, but majority also contain T cells; there is a 10-fold increase in T cell-containing infiltrates in transgenic B cell-deficient mice
• some infiltrates become medium or large-sized and are composed mainly of CD4+ T cells




Genotype
MGI:3767451
cx21
Allelic
Composition
Faslpr/Faslpr
Ighmtm1Cgn/Ighmtm1Cgn
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * MRL/Mp
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Faslpr mutation (39 available); any Fas mutation (82 available)
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• a transitional block in early B cell development in evident in bone marrow; pre-B cells are decreased in number
• number of Ig-positive B cells in spleen are 10- to 20-fold lower than in wild-type or Faslpr mice
• cell outgrowth in lymphadenopathy is dominated by Tcrb/B220+ cells
• at 8-10 weeks of age, mice develop significant lymphadenopathy
• mice fail to respond to T cell-dependent (OVA) or T cell-independent (dextra) antigenic stimulation and do not produce serum specific antibodies to these antigens
• levels of IgG2a and IgA are elevated compared to wild-type mice; significant levels (up to 10-fold) of serum antibodies have the gamma light chain isotype compared to control
• levels are much lower than in controls, comparable to Igh-6 single nulls
• mice have high titers of chromatin antibodies compared to controls and titer increased with age; anti-cardiolipin antibodies are increased in serum in 40% of double mutants

hematopoietic system
• a transitional block in early B cell development in evident in bone marrow; pre-B cells are decreased in number
• number of Ig-positive B cells in spleen are 10- to 20-fold lower than in wild-type or Faslpr mice
• cell outgrowth in lymphadenopathy is dominated by Tcrb/B220+ cells
• levels of IgG2a and IgA are elevated compared to wild-type mice; significant levels (up to 10-fold) of serum antibodies have the gamma light chain isotype compared to control
• levels are much lower than in controls, comparable to Igh-6 single nulls

homeostasis/metabolism
• mice show significant proteinuria

renal/urinary system
• mice show significant proteinuria




Genotype
MGI:3842821
cx22
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(TcraR28,TcrbR28)KRNDim/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * NOD * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(TcraR28,TcrbR28)KRNDim mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• arthritis does not occur in these mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
NOT rheumatoid arthritis DOID:7148 OMIM:180300
J:36815




Genotype
MGI:5437736
cx23
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(IghMyc)22Bri/0
Genetic
Background
involves: 129S2/SvPas * C57BL * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(IghMyc)22Bri mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm




Genotype
MGI:6383231
cx24
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Ptpn6me-v/Ptpn6me-v
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Ptpn6me-v mutation (3 available); any Ptpn6 mutation (49 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3629519
cx25
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tnftm2Gkl/Tnf+
Genetic
Background
involves: 129S/SvEv * 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tnftm2Gkl mutation (1 available); any Tnf mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• development and severity of inflammatory bowel disease are similar to Tnftm2Gkl/+, wild-type B2m controls

digestive/alimentary system
• development and severity of inflammatory bowel disease are similar to Tnftm2Gkl/+, wild-type B2m controls




Genotype
MGI:3581965
cx26
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Igh-VB1-8/Igh-6m)1Mjsk/?
Genetic
Background
NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(Igh-VB1-8/Igh-6m)1Mjsk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• female Igh-6-deficient transgenic mice show a 7-fold increase in the incidence of (blood glucose >250 mg/dl) diabetes compared with nontransgenic littermates

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:93190




Genotype
MGI:3687129
cx27
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Ighmtm1Cgn/Ighmtm1Cgn
Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell
Genetic
Background
NOD.Cg-Ighmtm1Cgn H2-Ab1b-tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (83 available)
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• magnitude of cardiac enlargement is similar to NOD transgenic H2-Ab1-null, Igh-6-sufficient mice
• appearance of heart block is not significantly different from NOD transgenic H2-Ab1-null, Igh-6-sufficient mice
• at 22 weeks, mice show mononuclear cell infiltrates in heart walls

immune system
• at 22 weeks, mice show mononuclear cell infiltrates in heart walls

growth/size/body
• magnitude of cardiac enlargement is similar to NOD transgenic H2-Ab1-null, Igh-6-sufficient mice




Genotype
MGI:3623595
cx28
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Igh-6/Igh-V125)2Jwt/0
Tg(Igk-C/Igk-V125)1Jwt/0
Genetic
Background
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V125)2Jwt Tg(Igk-C/Igk-V125)1Jwt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(Igh-6/Igh-V125)2Jwt mutation (1 available)
Tg(Igk-C/Igk-V125)1Jwt mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• by 40 weeks, pancreata of transgenic mice show extensive infiltrates; at 6 weeks, in the early prediabetic period, the incidence of infiltration is 40-50%

immune system
• by 40 weeks, pancreata of transgenic mice show extensive infiltrates; at 6 weeks, in the early prediabetic period, the incidence of infiltration is 40-50%




Genotype
MGI:3623596
cx29
Allelic
Composition
Ighmtm1Cgn/Ighm+
Tg(Igh-6/Igh-V125)2Jwt/0
Tg(Igk-C/Igk-V125)1Jwt/0
Genetic
Background
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V125)2Jwt Tg(Igk-C/Igk-V125)1Jwt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(Igh-6/Igh-V125)2Jwt mutation (1 available)
Tg(Igk-C/Igk-V125)1Jwt mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• the percentage of islets infiltrated is slightly increased in Igh-6-heterozygous transgenic mice

immune system
• the percentage of islets infiltrated is slightly increased in Igh-6-heterozygous transgenic mice
• transgenic females heterozygous for Igh-6 develop diabetes (2 consecutive blood glucose measurements >200 mg/dl) at a slightly earlier time (12 weeks) than homozygous transgenic females but the incidence is the same by 17 weeks

homeostasis/metabolism




Genotype
MGI:3623593
cx30
Allelic
Composition
Ighmtm1Cgn/Ighm+
Tg(Igh-6/Igh-V281)3Jwt/0
Genetic
Background
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V281)3Jwt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(Igh-6/Igh-V281)3Jwt mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• the percentage of islets infiltrated is slightly greater in transgenic mice heterozygous for Igh-6

immune system
• the percentage of islets infiltrated is slightly greater in transgenic mice heterozygous for Igh-6

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:91865




Genotype
MGI:3623592
cx31
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(Igh-6/Igh-V281)3Jwt/0
Genetic
Background
NOD.Cg-Ighmtm1Cgn Tg(Igh-6/Igh-V281)3Jwt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(Igh-6/Igh-V281)3Jwt mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• by 40 weeks, pancreata of transgenic mice show extensive infiltrates; at 6 weeks, in the early prediabetic period, the incidence of infiltration is 40-50% slightly less than mice carrying the V281 transgene; the percentage of islets infiltrated is slightly greater in transgenic mice heterozygous for Igh-6

immune system
• by 40 weeks, pancreata of transgenic mice show extensive infiltrates; at 6 weeks, in the early prediabetic period, the incidence of infiltration is 40-50% slightly less than mice carrying the V281 transgene; the percentage of islets infiltrated is slightly greater in transgenic mice heterozygous for Igh-6




Genotype
MGI:3793299
cx32
Allelic
Composition
Ighmtm1Cgn/Ighmtm1Cgn
Tg(IghelMD4)4Ccg/Tg(IghelMD4)4Ccg
Genetic
Background
NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighmtm1Cgn mutation (17 available); any Ighm mutation (56 available)
Tg(IghelMD4)4Ccg mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD
• mice have low levels of insulitis starting at 12 weeks of age with a mean disease score of 1.62 compared to non-transgenic NOD mice that have a mean score of 3.01 at this age
• the number of CD8 T cells found in the spleen is half that of non-transgenic NOD mice
• the number but not the proportion of B cells found in the spleen is twice that of non-transgenic NOD mice
• all of the B cells express the transgenic IgM B cell receptor specific for hen egg lysozyme
• purified B cells fail to stimulate T cells from non-transgenic NOD mice when cultured together in the presence of the diabetes autoantigen GAD
• 16.7% of female mice develop diabetes by 21 weeks of age compared to control NOD mice that have an incidence rate of 95.5% at this age
• mice with lymphosarcomas were not included in the analysis

neoplasm
• lymphosarcomas are present in the majority of mice with development starting at 20 weeks of age

hematopoietic system
• T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD
• the number of CD8 T cells found in the spleen is half that of non-transgenic NOD mice
• the number but not the proportion of B cells found in the spleen is twice that of non-transgenic NOD mice
• all of the B cells express the transgenic IgM B cell receptor specific for hen egg lysozyme
• purified B cells fail to stimulate T cells from non-transgenic NOD mice when cultured together in the presence of the diabetes autoantigen GAD

endocrine/exocrine glands
• mice have low levels of insulitis starting at 12 weeks of age with a mean disease score of 1.62 compared to non-transgenic NOD mice that have a mean score of 3.01 at this age

cellular
• T cells fail to proliferate when splenocytes are cultured in vitro with the diabetes autoantigen GAD

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
NOT type 1 diabetes mellitus DOID:9744 OMIM:222100
J:80859





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory