About   Help   FAQ
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 (55 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 (55 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 (55 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 (55 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 (55 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 (55 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 (55 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 (55 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 (55 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 (55 available)
Yaa mutation (18 available); any Yaa mutation (21 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 (55 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 (55 available)
Ightm3Tim mutation (0 available); any Igh mutation (43 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 (55 available)
Trex1tm1Tld mutation (2 available); any Trex1 mutation (22 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 (55 available)
Unc93b1tm1.1Kmiy mutation (6 available); any Unc93b1 mutation (38 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 (36 available)
Ighmtm1Cgn mutation (17 available); any Ighm mutation (55 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 (55 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 (55 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 (55 available)
Tgfb1tm1Doe mutation (4 available); any Tgfb1 mutation (34 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 (55 available)
Tgfb1tm1Doe mutation (4 available); any Tgfb1 mutation (34 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 (55 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 (55 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 (55 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 (55 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 (55 available)
Ptpn6me-v mutation (3 available); any Ptpn6 mutation (47 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 (55 available)
Tnftm2Gkl mutation (1 available); any Tnf mutation (46 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 (55 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 (81 available)
Ighmtm1Cgn mutation (17 available); any Ighm mutation (55 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 (55 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 (55 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 (55 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 (55 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 (55 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





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/16/2024
MGI 6.23
The Jackson Laboratory