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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ifngtm1Ts
targeted mutation 1, Timothy Stewart
MGI:1857184
Summary 32 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ifngtm1Ts/Ifngtm1Ts B6.129S7-Ifngtm1Ts MGI:4365971
hm2
Ifngtm1Ts/Ifngtm1Ts B6.129S7-Ifngtm1Ts/J MGI:3696100
hm3
Ifngtm1Ts/Ifngtm1Ts C.129S7(B6)-Ifngtm1Ts/J MGI:4839056
hm4
Ifngtm1Ts/Ifngtm1Ts C.129S7-Ifngtm1Ts MGI:4838443
hm5
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd MGI:3693883
hm6
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd * A/WySn * C57BL/10SnSg * Swiss MGI:4843967
hm7
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd * BALB/c MGI:4838445
hm8
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd * C57BL/6 MGI:3587743
hm9
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd * C57BL/6J MGI:4838441
hm10
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd * DBA/1 * MRL/Mp MGI:4839050
hm11
Ifngtm1Ts/Ifngtm1Ts involves: 129S7/SvEvBrd * NOD MGI:4838444
hm12
Ifngtm1Ts/Ifngtm1Ts NOD.129S7(B6)-Ifngtm1Ts/DvsJ MGI:3623449
hm13
Ifngtm1Ts/Ifngtm1Ts NOD.129S7(B6)-Ifngtm1Ts Prkdcscid MGI:3623448
hm14
Ifngtm1Ts/Ifngtm1Ts NOD.129S7-Ifngtm1Ts MGI:3622412
cn15
Ifngtm1Ts/Ifngtm1Ts
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
Tg(Cd4-cre)1Cwi/0
involves: 129 * C57BL/6 * DBA/2 * NOD * SJL MGI:5514242
cn16
Foxo1tm1Flv/Foxo1tm1Flv
Ifngtm1Ts/Ifngtm1Ts
Foxp3tm4(YFP/icre)Ayr/Foxp3+
involves: 129S1/Sv * 129S6/SvEvTac * 129S7/SvEvBrd * 129X1/SvJ MGI:5448156
cx17
Apoetm1Unc/Apoetm1Unc
Ifngtm1Ts/Ifngtm1Ts
B6.129-Apoetm1Unc Ifngtm1Ts MGI:4938323
cx18
Ifngtm1Ts/Ifngtm1Ts
Ldlrtm1Her/Ldlrtm1Her
B6.129S7-Ldlrtm1Her Ifngtm1Ts MGI:4867042
cx19
Csf2tm1Mlg/Csf2tm1Mlg
Ifngtm1Ts/Ifngtm1Ts
Il3tm1Glli/Il3tm1Glli
B6.129S-Csf2tm1Mlg Il3tm1Glli Ifngtm1TsIfngtm1Ts MGI:5431918
cx20
Ifngtm1Ts/Ifngtm1Ts
Tgfb1tm1Doe/Tgfb1tm1Doe
C.129-Ifngtm1Ts Tgfb1tm1Doe MGI:3721950
cx21
Ifngtm1Ts/Ifngtm1Ts
Prf1tm1Sdz/Prf1tm1Sdz
C.Cg-Prf1tm1Sdz Ifngtm1Ts MGI:4867045
cx22
Ifngtm1Ts/Ifngtm1Ts
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Tnfrsf1btm1Mwm/Tnfrsf1btm1Mwm
involves: 129P2/OlaHsd * 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 MGI:4843969
cx23
Ifngtm1Ts/Ifng+
Socs1tm1Wehi/Socs1tm1Wehi
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 MGI:4850158
cx24
Ifngtm1Ts/Ifngtm1Ts
Socs1tm1Wehi/Socs1tm1Wehi
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 MGI:4430638
cx25
Csf2tm1Dran/Csf2tm1Dran
Ifngtm1Ts/Ifngtm1Ts
Il3tm1Glli/Il3tm1Glli
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 MGI:3586344
cx26
Ifngtm1Ts/Ifngtm1Ts
Socs1tm1Jni/Socs1tm1Jni
involves: 129S7/SvEvBrd MGI:3783715
cx27
Ifngtm1Ts/Ifngtm1Ts
Nlrp1aNeut1/Nlrp1aNeut1
involves: 129S7/SvEvBrd * C57BL/6 MGI:5474288
cx28
Ifngtm1Ts/Ifngtm1Ts
Tg(SFTPC-Il18)AThos/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6N * DBA/2 MGI:5688500
cx29
Faslpr/Faslpr
Ifngtm1Ts/Ifngtm1Ts
involves: 129S7/SvEvBrd * DBA/1 * MRL/Mp MGI:4839049
cx30
Ifngtm1Ts/Ifngtm1Ts
Tnftm2Gkl/Tnf+
involves: 129S/SvEv * 129S7/SvEvBrd * C57BL/6J MGI:3629594
cx31
Faslpr/Faslpr
Ifngtm1Ts/Ifng+
MRL.Cg-Ifngtm1Ts Faslpr MGI:3801419
cx32
Faslpr/Faslpr
Ifngtm1Ts/Ifngtm1Ts
MRL.Cg-Ifngtm1Ts Faslpr MGI:3801418


Genotype
MGI:4365971
hm1
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
B6.129S7-Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands

mortality/aging
• sudden death occurs 5 to 7 weeks after infection with Leishmania major (J:18801)
• die earlier after inoculation with Toxoplasma gondii (strain ME49) compared to wild-type controls (J:110826)
• higher mortality is seen following infection with JHMV compared to wild-type controls
• Background Sensitivity: in mice on a C57BL/6 background compared to mice on a BALB/c background

neoplasm
• Background Sensitivity: 50% of mice on a congenic C57BL/5 background develop disseminated lymphomas compared to 0% of mice on a congenic BALB/c background
• most lymphomas are diffuse large cell lymphomas
• in a few mice
• Background Sensitivity: in mice on a C57BL/6 background compared to mice on a BALB/c background

immune system
• increase in the number of CD8+ cells in the white matter tracts of JHMV infected mice compared to similarly infected wild-type controls at 7 and 14 days post infection
• immature B cells fail to be excluded from the lymph nodes
• after infection with Leishmania major
• after infection with Leishmania major (J:18801)
• 5-fold increase in the serum levels of JHMV specific IgG1 at 14 days post infection compared to infected wild-type controls (J:112048)
• after infection with Leishmania major
• after infection with Leishmania major
• significant increase in the numbers of immature B cells in the lymph nodes
• after infection with Leishmania major the number of lymphocytes producing IL4 increases unlike in control mice where the number of lymphocytes producing IFNG increases (J:18801)
• following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice (J:110826)
• cervical lymph node cells from JHMV infected mice (7 days post infection) secrete more IL10 in response to JHMV antigen compared to cells from similarly infected wild-type mice
• cervical lymph node cells from JHMV infected mice secrete more IL2 in response to JHMV antigen compared to cells from similarly infected wild-type mice
• cervical lymph node cells from JHMV infected mice (7 days post infection) secrete more IL5 in response to JHMV antigen compared to cells from similarly infected wild-type mice
• after infection with Leishmania major mice display minimal Th1 type responses and increased Th2 type responses (J:18801)
• after infection with Leishmania major levels of IgG1 and IgE are increased while levels of IgG2a and IgG3 remain low (J:18801)
• following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice (J:110826)
• develop progressive infection characterized by large lesions at the site of inoculation and sudden death 5 to 7 weeks after infection with Leishmania major
• numbers of parasites present in the footpads are substantially increased compared to wild-type and heterozygous controls
• sudden death occurs 5 to 7 weeks after infection with Leishmania major (J:18801)
• die earlier after inoculation with Toxoplasma gondii (strain ME49) compared to wild-type controls (J:110826)
• following infection with the JHM strain of mouse hepatitis virus (JHMV) mice display a slower clinical recovery and higher viral titers in the central nervous system compared to wild-type controls
• however, no differences are found in JHMV specific cytotoxic T lymphocyte activity
• at 14 days post infection with JHMV a 10 fold increase in the number of viral antigen positive cells is detected in the brain with most of the infected cells being oligodendrocytes
• higher mortality is seen following infection with JHMV compared to wild-type controls
• after immunosuppressive treatment (anti-CD4 and anti-CD8 mAbs) allografts (BALB/c, H2-Ab1bm12 continue to display myocardial rejection at week 12 but do not display graft arterial disease, in contrast wild-type mice at week 12 display low levels of rejection but develop coronary arteriopathy

hematopoietic system
• increase in the number of CD8+ cells in the white matter tracts of JHMV infected mice compared to similarly infected wild-type controls at 7 and 14 days post infection
• immature B cells fail to be excluded from the lymph nodes
• after infection with Leishmania major
• after infection with Leishmania major (J:18801)
• 5-fold increase in the serum levels of JHMV specific IgG1 at 14 days post infection compared to infected wild-type controls (J:112048)
• after infection with Leishmania major
• after infection with Leishmania major




Genotype
MGI:3696100
hm2
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
B6.129S7-Ifngtm1Ts/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls
• die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
• most mice die by 9 days after infection with 1x106 Cryptosporidium parvum oocysts

immune system
N
• do not exhibit defects on either IgE isotype switch or IgE production
• 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
• 5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice
• following infection with BCG
• in the blood, bone marrow and spleen following infection with BCG
• unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers
• following infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
• develop splenomegaly after infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
• spleens become paler as BCG infection proceeds
• increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
• following infection with BCG
• in C. parvum infected mice
• increase in IL12 and decrease in IL10 secretion following LPS stimulation
• enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro
• enhancement in LPS induced dendritic cell migration to the spleen
• enhancement in hapten induced Langerhan cell migration to the draining lymph nodes
• dendritic cells show a greater ability to stimulate T cell proliferation in vitro
• in OVA fed mice only a modest decrease in the delayed type hypersensitivity response to injected OVA is seen in contrast this reaction is strongly decreased in similarly treated wild-type controls
• display a more severe delayed type hypersensitivity reaction in response to sheep IgG
• the magnitude of the OVA specific antibody response to subcutaneous OVA challenge is reduced
• however, following oral OVA exposure OVA antibody levels in response to subcutaneous OVA challenge are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels
• IgG responses are restricted to IgG1 and IgG2b
• splenocytes fail to produce IFN-gamma in response to H. pylori antigen stimulation
• splenocytes from Helicobacter pylori infected mice produce 4-fold less IL-10 when cultured in the presence of H. pylori antigen (J:120556)
• by bone marrow dendritic cells following LPS stimulation (J:134949)
• by bone marrow dendritic cells following LPS stimulation
• splenocytes from Helicobacter pylori infected mice produce significantly more IL-4 than splenocytes from wild-type controls when cultured in the presence of H. pylori antigen
• oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent subcutaneous exposure to the same antigen
• increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes
• following infection with BCG mice display an increased bacterial load throughout the infect in contrast to wild-type mice where bacterial numbers peak at 17 days post infection and decline thereafter
• following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen
• die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
• Background Sensitivity: mice on a C57BL/6 background lose weight and develop soft gelatinous stools over the course of a C. parvum infection while mice on a BALB/c background do not
• Background Sensitivity: in C. parvum infected mice on a C57BL/6 background, but not on a BALB/c background, the gastrointestinal tract is heavily colonized with parasites, the small intestines are distended and filled with gelatinous fluid, mesenteric lymph nodes are enlarged and in about 50% of mice gallbladders are enlarged
• most mice die by 9 days after infection with 1x106 Cryptosporidium parvum oocysts
• decrease in survival times of heart transplants from CBA mice after a 30 day course of anti-CD4 and anti-CD8 mAb
• only 10% of heart grafts survive more than 100 days compared to 36% of grafts in wild-type mice

behavior/neurological
• Background Sensitivity: increase in the number of defecations in a novel environment compared to wild-type controls in mice on a C57BL/6 background but not in mice on a BALB/c background
• the number of rearings is decreased in a novel environment
• initial locomotor activity is decreased; however, overall distance traveled is not different from controls
• Background Sensitivity: increase in the number of defecations following a sound stimulus suggesting an enhancement of fear related responses in mice on a C57BL/6 background but not in mice on a BALB/c background
• prolonged freeze time and longer time to return to normal open field activity patterns following a startle stimulus relative to wild-type controls
• make fewer entries and spend less time in the open arms of an elevated maze relative to wild-type controls
• in a novel environment

cellular
• enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro
• enhancement in LPS induced dendritic cell migration to the spleen
• 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
• unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase the production of reactive oxygen species in hepatocytes

renal/urinary system
• 1 day after induction of accelerated antiglomerular basement membrane nephritis no increase in total urinary nitrate or nitrate levels is detected unlike in similarly treated wild-type controls
• increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis
• increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes

homeostasis/metabolism
• increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
• following infection with BCG
• unlike in wild-type mice, treatment with LPS and DGalN fails to increase nitric oxide levels
• 1 day after induction of accelerated antiglomerular basement membrane nephritis no increase in total urinary nitrate or nitrate levels is detected unlike in similarly treated wild-type controls
• increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis
• increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls
• decrease in the number and area of regenerating muscle fibers 5 and 10 days after muscle injury
• fibrotic lesions are sometimes seen after injury
• 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
• following a 48 h exposure to hyperoxia (98-99% oxygen) neutrophil migration into the lung air space and the increase in pulmonary alveolar permeability are decreased indicating a decrease susceptibility to the early phase of hyperoxia induced lung injury
• however, after 84 h of exposure to hyperoxia these measures are not different from similarly exposed to wild-type controls

muscle
• fibrotic lesions are sometimes seen after injury
• decrease in the number and area of regenerating fibers 5 and 10 days after injury
• fibrotic lesions are sometimes seen after injury
• however, prior to injury no difference in muscle fiber morphology are detected

digestive/alimentary system
• 5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice

hematopoietic system
• 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
• following infection with BCG
• following infection with BCG
• in the blood, bone marrow and spleen following infection with BCG
• unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers
• following infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
• develop splenomegaly after infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
• spleens become paler as BCG infection proceeds
• IgG responses are restricted to IgG1 and IgG2b




Genotype
MGI:4839056
hm3
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
C.129S7(B6)-Ifngtm1Ts/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis

immune system
• the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
• after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
• following infection with BCG
• in the blood, bone marrow and spleen following infection with BCG
• following infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
• develop splenomegaly after infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
• spleens become paler as BCG infection proceeds
• increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
• following infection with BCG
• decrease in the cytotoxicity of NK cells from mice primed with rIL12
• decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation
• uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
• C26 cells induce slightly reduced CTL activity compared to the response in similarly treat wild-type mice
• exposure to rIL12 fails to prime macrophages against subsequent LPS exposure
• lymphocytes form C25/Il12 cell primed mice produce about 3 fold higher levels of CSF2
• in C26/Il12 tumors CD4+ T cells are more numerous relative to CD8+ T cells, in tumors in wild-type mice CD8+ T cells are more numerous
• following infection with BCG mice display an increased bacterial load throughout the infect in contrast to wild-type mice where bacterial numbers peak at 17 days post infection and decline thereafter
• following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen
• die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
• Background Sensitivity: unlike mice on a C57BL/6 background, mice on a BALB/c background do not lose weight, show any change in stool consistency, or display heavy parasitic loads in the gastrointestinal tract over the course of a C. parvum infection

behavior/neurological
• the number of rearings is decreased in a novel environment
• Background Sensitivity: unlike mice on a C57BL/6 background, no increase in the number of defecations in a novel environment or following a sound stimulus is seen in mice on a BALB/c background, compared to wild-type controls
• prolonged freeze time following a startle stimulus relative to wild-type controls
• Background Sensitivity: no increase in the number of defecations following a sound stimulus is seen in mice on a BALB/c background unlike mice on a C57BL/6 background
• in a novel environment

neoplasm
• when injected with 5 x 105 C26/Il12 cells only a few mice are able to reject the tumor, in contrast 80 - 100% of wild-type mice reject the tumor
• in C26/Il12 derived tumors, tumor vessels are more numerous and thinner compared to vessels in tumors in wild-type mice
• tumor onset is accelerated in 40% of mice injected with 5 x 104 C26 carcinoma cells transduced with Il12 genes (C26/Il12) compared to similarly treated wild-type mice
• however, no difference is detected when parental C26 cells are used

reproductive system
• after gestational day 10 the intercellular composition of the decidua changes suggesting accumulations of fluid and extracellular matrix, areas of necrosis are present and a lack of decidual cellularity is apparent
• the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
• after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
• decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation
• uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
• decrease in litter size and increase in the number of resorbed embryos in the first litter
• no difference in litter size or number of resorbed embryos is detected in subsequent pregnancies
• phenotype is independent of the genotype of the embryos

homeostasis/metabolism
• increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
• following infection with BCG

embryo
• after gestational day 10 the intercellular composition of the decidua changes suggesting accumulations of fluid and extracellular matrix, areas of necrosis are present and a lack of decidual cellularity is apparent
• the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
• after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls

hematopoietic system
• the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
• after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
• following infection with BCG
• following infection with BCG
• in the blood, bone marrow and spleen following infection with BCG
• following infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
• develop splenomegaly after infection with BCG
• following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
• spleens become paler as BCG infection proceeds
• decrease in the cytotoxicity of NK cells from mice primed with rIL12
• decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation
• uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
• C26 cells induce slightly reduced CTL activity compared to the response in similarly treat wild-type mice
• exposure to rIL12 fails to prime macrophages against subsequent LPS exposure

endocrine/exocrine glands
• the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
• after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls




Genotype
MGI:4838443
hm4
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
C.129S7-Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• in a few mice, with a very late onset
• all are well differentiated papillary adenocarcinomas

mortality/aging
• the LD50 for Listeria monocytogenes infection is 10 CFU compared to greater than 104 CFU for wild-type and heterozygous controls
• however the LD50 for a mutant strain of L. monocytogenes (DP-L1942) is similar in homozygous mice and controls
• following vaccination mice are able to develop resistance to L. monocytogenes infection
• die within 9 days of inoculation with T. gondii (strain ME49) unlike controls which survive more than 30 days
• highly susceptible to the normally avirulent T. gondii isolate, ts4

immune system
• the magnitude of the OVA specific antibody is reduced
• following oral OVA exposure OVA antibody levels are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels
• IgG responses are restricted to IgG1 and IgG2b
• following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
• following infection with T. gondii (irradiate RH strain) splenocytes produce more IL-5 compared to similar cultures from wild-type mice
• oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent exposure to the same antigen
• incidence rate (17 of 24 compared to 1 of 16 in controls) and severity are increased compared to contols immunization results in about a 30% mortality rate
• immunized mice display meningeal and perivascular inflammatory infiltrates in the spinal cord and brain similar to those seen in susceptible strains like SJL/J
• following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
• the LD50 for Listeria monocytogenes infection is 10 CFU compared to greater than 104 CFU for wild-type and heterozygous controls
• however the LD50 for a mutant strain of L. monocytogenes (DP-L1942) is similar in homozygous mice and controls
• following vaccination mice are able to develop resistance to L. monocytogenes infection
• dramatic increase in the number of infected cells expansion of the tissues infected following inoculation with Toxoplasma gondii (strain ME49)
• 5 days after inoculation with T. gondii (strain ME49) peritoneal exudates contain a more pronounced increase in the numbers of granulocytes, eosinophils, and mast cells compared to similarly infected wild-type controls
• IL-2 production in response to infection is similar to controls
• die within 9 days of inoculation with T. gondii (strain ME49) unlike controls which survive more than 30 days
• highly susceptible to the normally avirulent T. gondii isolate, ts4

neoplasm
N
• Background Sensitivity: unlike mice on a congenic C57BL/6 background, mice on a BALB/c background do not develop disseminated lymphomas
• in a few mice, with a very late onset
• all are well differentiated papillary adenocarcinomas
• Background Sensitivity: in mice on a BALB/c background compared to mice on a C57BL/6 background

hematopoietic system
• IgG responses are restricted to IgG1 and IgG2b




Genotype
MGI:3693883
hm5
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival time following infecting with virulent Mycobacterium tuberculosis is 15 days compared to over 60 days for wild-type controls
• treatment with exogenous IFNG improves survival
• more than 70% of mice infected on the cornea with herpes simplex virus type 1 (HSV-1) at a dose of 105 TCID50 (50% tissue culture infective dose) infectious particles die

immune system
• in mice with acute or chronic HSV-1 infection the ratio of IgG2a to IgG1 is dramatically reduced compared to BALB/c wild-type mice
• following infection with type A influenza
• activated splenic and liver NK cells are less efficient in their killing of 4T1 or Renca tumor target cells
• T cells from mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide show more IL-17a expressing cells and greater IL-17a production after MOG restimulation than controls; IL-4 is not detectable in these cells
• the magnitude of the delayed type hypersensitive response in mice after HSV-1 infection is reduced compared to BALB/c wild-type controls
• following culturing of IL-17 producing T cells in vitro, IL-17 production is twice as high as in similarly treated wild-type cells
• the magnitude of the delayed type hypersensitive response in mice after HSV-1 infection is reduced compared to BALB/c wild-type controls (J:29170)
• display an increased IgG1 antibody response to type A influenza infection (J:110721)
• 14 days after infection with virulent Mycobacterium tuberculosis serum levels of reactive nitrogen intermediates are very low, unlike in wild-type controls (J:110856)
• at 14 days after infection with virulent Mycobacterium tuberculosis, 10- 100 fold more viable bacteria are found in the organs compared to organs of wild-type controls
• at 14 days after infection with virulent Mycobacterium tuberculosis, about 90% of the granulomas in the liver and 20% of the granulomas in the spleen are necrotic
• treatment with exogenous IFNG decreases the bacterial load
• mean survival time following infecting with virulent Mycobacterium tuberculosis is 15 days compared to over 60 days for wild-type controls
• treatment with exogenous IFNG improves survival
• at 5 - 8 days post infection mice develop more severe conjunctivitis, periocular skin lesions, corneal opacity, and anterior chamber exudate following infection with HSV-1 relative to wld-type BALB/c controls infected with a higher dose of virus
• infectious virus is detected up to 10 days post infection with HSV-1 in mutants compared to up to 4 or days post infection in wild-type BAL/c mice or littermate controls, respectively
• more than 70% of mice infected on the cornea with herpes simplex virus type 1 (HSV-1) at a dose of 105 TCID50 (50% tissue culture infective dose) infectious particles die

vision/eye
• corneal injection of a plasmid encoding short hairpin RNA targeting the C terminus of the secreted form of Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice

homeostasis/metabolism
• T cells from mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide show more IL-17a expressing cells and greater IL-17a production after MOG restimulation than controls; IL-4 is not detectable in these cells

cardiovascular system
• corneal injection of a plasmid encoding short hairpin RNA targeting the C terminus of the secreted form of Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice

hematopoietic system
• in mice with acute or chronic HSV-1 infection the ratio of IgG2a to IgG1 is dramatically reduced compared to BALB/c wild-type mice
• following infection with type A influenza
• activated splenic and liver NK cells are less efficient in their killing of 4T1 or Renca tumor target cells




Genotype
MGI:4843967
hm6
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * A/WySn * C57BL/10SnSg * Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• relative to wild-type controls
• however, mercury treatment does not result in an increase in IgG1 levels
• decrease in the induction of IgG in response to low levels of antigen ((4-hydroxy-3 nitrophenyl)acetyl)
• following exposure to HgCl2 for 4 weeks, relative to similarly treated wild-type and heterozygous mice
• resistant to mercury induced autoimmune response

homeostasis/metabolism
• resistant to mercury induced autoimmune response

hematopoietic system
• relative to wild-type controls
• however, mercury treatment does not result in an increase in IgG1 levels
• decrease in the induction of IgG in response to low levels of antigen ((4-hydroxy-3 nitrophenyl)acetyl)
• following exposure to HgCl2 for 4 weeks, relative to similarly treated wild-type and heterozygous mice




Genotype
MGI:4838445
hm7
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * BALB/c
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• no difference in survival, tissue damage or spread of infection following infection with the opportunistic fungal pathogen Candida albicans is detected relative to wild-type controls
• ovalbumin challenge fails to significantly potentiate ovalbumin specific IgE levels, unlike in wild-type controls
• the eosinophilic response in ovalbumin challenged mice is reduced compared to wild-type controls
• mice are able to clear infectious Murine gammaherpesvirus 68 (MHV-68) from their lungs but with a slight delay relative wild-type mice
• no differences are detected in the frequency of latently infected cells, the generation of cytotoxic T cells, the infection induced cytokine profile, or the recruitment or proliferation of cells into inflammatory sites

respiratory system
• ovalbumin challenge fails to induce airway hyperresponsiveness unlike in wild-type mice
• in saline challenged mice relative to wild-type controls

hematopoietic system
• ovalbumin challenge fails to significantly potentiate ovalbumin specific IgE levels, unlike in wild-type controls




Genotype
MGI:3587743
hm8
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice are able to clear infections of Pneumocystis carinii, similar to controls
• splenocytes from BCG infected mice exhibit increased proliferation in response to Con A
• significantly lower resting splenic NK cell activity (J:66802)
• recruitment of NK cells to the liver by recombinant murine IL12 is impaired (J:115033)
• however, the recruitment of T cells by IL12 is not impaired (J:115033)
• macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge
• macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge
• macrophages from BCG infected mice exhibit reduced class II expression
• exposure to UVA and UVB fails to significantly reduce the UVB induced suppression of the type IV hypersensitivity reaction
• however, the type IV hypersensitivity reaction in the absence of UV exposure is similar to controls
• increased mortality following a sublethal dose of Mycobacterium bovis (BCG )
• mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice
• however, IFNG-competent alpha+CD4+ T cells promote experimental cerebral malaria
• mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice
• reduced surival of cardiac grafts relative to controls

neoplasm
• following treatment with alphaGalCer, mice fail to exhibit a reduction in the number of B16F10 tumors metastasizing to the lungs unlike similarly treated wild-type mice
• tumor-bearing mice treated with Th-17-polarized cells from Tg(Tcra,Tcrb)9Rest cells show increased tumor rejection compared to controls

craniofacial
• modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

skeleton
• modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

hematopoietic system
• splenocytes from BCG infected mice exhibit increased proliferation in response to Con A
• significantly lower resting splenic NK cell activity (J:66802)
• recruitment of NK cells to the liver by recombinant murine IL12 is impaired (J:115033)
• however, the recruitment of T cells by IL12 is not impaired (J:115033)
• macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge
• macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge
• macrophages from BCG infected mice exhibit reduced class II expression

integument
• following exposure to UVA and UVB mice fail to develop significant erythema unlike wild-type controls
• however, the increase in skin fold thickness in response to UVB or UVA and UVB exposure is not significantly different from controls

cellular
• splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

mortality/aging
• mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice

Mouse Models of Human Disease
OMIM ID Ref(s)
Malaria, Susceptibility to 611162 J:189794




Genotype
MGI:4838441
hm9
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• after infection with a normally sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice become severely ill and need to be euthanized

immune system
• following infection with a sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice develop widespread infection with high numbers of bacteria in multiple tissues and obvious bacteremia
• by 4 weeks after aerosol infection with the virulent Erdam strain of Mycobacterium tuberculosis mice display multifocal necrotic areas contain high numbers of bacteria in the spleen, liver, lungs and kidneys
• after infection with a normally sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice become severely ill and need to be euthanized




Genotype
MGI:4839050
hm10
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * DBA/1 * MRL/Mp
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• at 3 months of age relative to wild-type controls
• at 3 and 7-8 months of age relative to wild-type controls
• at 3 and 7-8 months of age relative to wild-type controls
• at 3 months of age relative to wild-type controls
• at 3 months of age relative to wild-type controls
• older mice appear to be protected from end organ disease relative to wild-type controls
• levels of anti-snRNP antibodies are decreased at 3 but not at 7-8 months of age relative to wild-type controls
• at 3 and 7-8 months of age relative to wild-type controls
• at 3 months of age relative to wild-type controls
• at 7 -8 months of age levels of anti-dsDNA antibodies are similar to wild-type controls but these antibodies fail to bind dsDNA containing kinetoplast of Crithidia luciliae substrates suggesting the antibodies are of low affinity

hematopoietic system
• at 3 months of age relative to wild-type controls
• at 3 and 7-8 months of age relative to wild-type controls
• at 3 and 7-8 months of age relative to wild-type controls
• at 3 months of age relative to wild-type controls
• at 3 months of age relative to wild-type controls




Genotype
MGI:4838444
hm11
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * NOD
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• Background Sensitivity: at generation N4 no difference is seen in the time course of diabetes development in females unlike in mice at generation N7




Genotype
MGI:3623449
hm12
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
NOD.129S7(B6)-Ifngtm1Ts/DvsJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• CD8+ T cells injected into Ifng-deficient NOD mice are less able to cause diabetes, due to impaired homing ability and impaired diapedesis
• when diabetic NOD splenocytes are transferred into mutant NOD mice, only 33% develop diabetes over the course of the observation period

endocrine/exocrine glands
• islet cells from Ifng-deficient NOD mice are less susceptible to insulin-specific CD8+ cell-induced toxicity

hematopoietic system
• CD8+ T cells injected into Ifng-deficient NOD mice are less able to cause diabetes, due to impaired homing ability and impaired diapedesis

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Insulin-Dependent; IDDM 222100 J:72818




Genotype
MGI:3623448
hm13
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
NOD.129S7(B6)-Ifngtm1Ts Prkdcscid
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• when diabetic NOD splenocytes are transferred into mutant NOD.scid mice only 23% of recipients become diabetic (determined by monitoring urine glucose level) 7 weeks after transfer, but 100% of wild-type NOD.Scid mice are diabetic within 5 weeks

Mouse Models of Human Disease
OMIM ID Ref(s)
Diabetes Mellitus, Insulin-Dependent; IDDM 222100 J:72818




Genotype
MGI:3622412
hm14
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
NOD.129S7-Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• Background Sensitivity: delay in the development of diabetes in females at generation N7 but not a generation N4
• however, the ultimate penetrance of the diabetes phenotype does not differ from wild-type controls and no gross differences in pancreatic inflammation are detected
• null animals challenged with CVB4 at 8 weeks of age show a retarded rate of diabetes (2 consecutive blood glucose measures >240 mg/dl) development compared to saline-treated controls; over the 25-week follow up period, about 30% of CVB4-exposed nulls develop disease versus around 90% of aline-treated controls




Genotype
MGI:5514242
cn15
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
Tg(Cd4-cre)1Cwi/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2 * NOD * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Tg(Cd4-cre)1Cwi mutation (4 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (15 available)
Tg(TcraBDC2.5,TcrbBDC2.5)1Doi mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• improved survival

immune system
N
• do not develop diabetes




Genotype
MGI:5448156
cn16
Allelic
Composition
Foxo1tm1Flv/Foxo1tm1Flv
Ifngtm1Ts/Ifngtm1Ts
Foxp3tm4(YFP/icre)Ayr/Foxp3+
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxo1tm1Flv mutation (0 available); any Foxo1 mutation (11 available)
Foxp3tm4(YFP/icre)Ayr mutation (1 available); any Foxp3 mutation (32 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• the lethal inflammatory phenotype is partially rescued

immune system
N
• regulatory T cells are able to suppress development of colitis in Rag1 null mice receiving na[?]ve T cells
• elevated numbers in the spleen and peripheral lymph nodes are partially rescued compared to in Foxo1tm1Flv/Foxo1tm1Flv Foxp3/Foxp3+ mice
• elevated numbers in the spleen and peripheral lymph nodes are partially rescued compared to in Foxo1tm1Flv/Foxo1tm1Flv Foxp3/Foxp3+ mice

hematopoietic system
• elevated numbers in the spleen and peripheral lymph nodes are partially rescued compared to in Foxo1tm1Flv/Foxo1tm1Flv Foxp3/Foxp3+ mice
• elevated numbers in the spleen and peripheral lymph nodes are partially rescued compared to in Foxo1tm1Flv/Foxo1tm1Flv Foxp3/Foxp3+ mice




Genotype
MGI:4938323
cx17
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
B6.129-Apoetm1Unc Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (68 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 50% of mice infused with angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng

cardiovascular system
• about 50% of mice infused with 1000 ng/kg*min angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng
• increase in the incidence of abdominal aorta aneurysyms in in mice infused with 500 ng/kg*min angiotensin-II compared to mutant mice wild-type for Ifng
• increase in the suprarenal aortic diameter in mice infused with 500 ng/kg*min angiotensin-II compared to mutant mice wild-type for Ifng

growth/size/body
• compared to mutant mice wild-type for Ifng




Genotype
MGI:4867042
cx18
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Ldlrtm1Her/Ldlrtm1Her
Genetic
Background
B6.129S7-Ldlrtm1Her Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Ldlrtm1Her mutation (19 available); any Ldlr mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• after 8 or 20 weeks on a cholesterol diet aortic lesion size is reduced compared to mice homozygous for Ldlrtm1Her alone

hematopoietic system
• increase in the proportion of T cells in the blood relative to controls homozygous for Ldlrtm1Her alone

immune system
• increase in the proportion of T cells in the blood relative to controls homozygous for Ldlrtm1Her alone




Genotype
MGI:5431918
cx19
Allelic
Composition
Csf2tm1Mlg/Csf2tm1Mlg
Ifngtm1Ts/Ifngtm1Ts
Il3tm1Glli/Il3tm1Glli
Genetic
Background
B6.129S-Csf2tm1Mlg Il3tm1Glli Ifngtm1TsIfngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csf2tm1Mlg mutation (1 available); any Csf2 mutation (13 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Il3tm1Glli mutation (1 available); any Il3 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system

endocrine/exocrine glands

homeostasis/metabolism
N
• significantly reduced fasting blood sugar, to levels similar to controls
• improved glucose tolerance

neoplasm




Genotype
MGI:3721950
cx20
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Tgfb1tm1Doe/Tgfb1tm1Doe
Genetic
Background
C.129-Ifngtm1Ts Tgfb1tm1Doe
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Tgfb1tm1Doe mutation (4 available); any Tgfb1 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive average of 32.9 days (range 23-66 days)

growth/size/body
• mice are smaller than littermate controls

liver/biliary system
N
• outwardly, livers show no visible abnormalities
• on necropsy, modest inflammatory expansion around portal tracts is observed in some animals

immune system
• on necropsy, modest inflammatory expansion around portal tracts is observed in some animals

homeostasis/metabolism
• in 4/5 mice >21 days of age, ALT plasma levels are elevated




Genotype
MGI:4867045
cx21
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Prf1tm1Sdz/Prf1tm1Sdz
Genetic
Background
C.Cg-Prf1tm1Sdz Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Prf1tm1Sdz mutation (10 available); any Prf1 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

neoplasm
• some lymphomas have an unusual histiocytic appearance with a pale eosinophilic cytoplasm
• incidence is increased and onset is earlier compared to mice homozygous for Prf1tm1Sdz alone
• incidence is increased and onset is earlier compared to mice homozygous for Prf1tm1Sdz alone




Genotype
MGI:4843969
cx22
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Tnfrsf1btm1Mwm/Tnfrsf1btm1Mwm
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (22 available)
Tnfrsf1btm1Mwm mutation (2 available); any Tnfrsf1b mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• in pulmonary lavage fluid 4 weeks after infection with Pneumocystis carinii relative to infected controls
• in pulmonary lavage fluid 4 weeks after infection with Pneumocystis carinii relative to infected controls
• in pulmonary lavage fluid 4 weeks after infection with Pneumocystis carinii relative to infected controls
• despite the absence of germinal centers the white pulp has distinct T and B cell areas
• grossly unidentifiable and histologically hypoplastic
• thin and lack primary and secondary cortical follicles
• develop severe inflammation 4 weeks after infection with Pneumocystis carinii
• 4 weeks after infection with Pneumocystis carinii lungs demonstrate severe infection indicating mice are unable to clear the infection
• 4 weeks after infection with Pneumocystis carinii pulmonary lavages contain about 10 fold higher numbers of leukocytes compared to similarly infected control mice

hematopoietic system
• in pulmonary lavage fluid 4 weeks after infection with Pneumocystis carinii relative to infected controls
• in pulmonary lavage fluid 4 weeks after infection with Pneumocystis carinii relative to infected controls
• in pulmonary lavage fluid 4 weeks after infection with Pneumocystis carinii relative to infected controls
• despite the absence of germinal centers the white pulp has distinct T and B cell areas

respiratory system
• develop severe inflammation 4 weeks after infection with Pneumocystis carinii




Genotype
MGI:4850158
cx23
Allelic
Composition
Ifngtm1Ts/Ifng+
Socs1tm1Wehi/Socs1tm1Wehi
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Socs1tm1Wehi mutation (0 available); any Socs1 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 8 of 12 mice died between 2 and 12 weeks of age, the remaining 4 survived
• 8 of 12 mice died between 2 and 12 weeks of age, the remaining 4 survived




Genotype
MGI:4430638
cx24
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Socs1tm1Wehi/Socs1tm1Wehi
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Socs1tm1Wehi mutation (0 available); any Socs1 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• unlike mice homozygous for Socs1tm1Wehi alone, double homozygous mice survive past weaning and are overtly healthy (J:57474)
• lethality observed in Socs1tm1Wehi homozygotes is rescued (J:70408)

reproductive system
• from day 16 of pregnancy, mice exhibit a higher density of lobuloalveolar units compared with wild-type mice
• however, proliferation of mammary epithelium is normal

endocrine/exocrine glands
• 8 of 12 mice have enlarged medulla
• however, unlike mice homozygous for Socs1tm1Wehi alone, the cortex is normal
• from day 16 of pregnancy, mice exhibit a higher density of lobuloalveolar units compared with wild-type mice
• however, proliferation of mammary epithelium is normal
• from day 16 of pregnancy, mice exhibit a higher density of lobuloalveolar units compared with wild-type mice
• however, lobuloalveolar density returns to normal by day 5 of lactation
• at day 18 of pregnancy, mammary glands produce more milk than in wild-type mice

cardiovascular system
• 2 of 12 mice show lymphoid cuffing of the lung vessels

hematopoietic system
N
• unlike mice homozygous for Socs1tm1Wehi alone, no hematological abnormalities are detected at 3 weeks of age
• 8 of 12 mice have enlarged medulla
• however, unlike mice homozygous for Socs1tm1Wehi alone, the cortex is normal

immune system
• 8 of 12 mice have enlarged medulla
• however, unlike mice homozygous for Socs1tm1Wehi alone, the cortex is normal

respiratory system
• 2 of 12 mice show lymphoid cuffing of the lung vessels

integument
• from day 16 of pregnancy, mice exhibit a higher density of lobuloalveolar units compared with wild-type mice
• however, proliferation of mammary epithelium is normal
• from day 16 of pregnancy, mice exhibit a higher density of lobuloalveolar units compared with wild-type mice
• however, lobuloalveolar density returns to normal by day 5 of lactation
• at day 18 of pregnancy, mammary glands produce more milk than in wild-type mice




Genotype
MGI:3586344
cx25
Allelic
Composition
Csf2tm1Dran/Csf2tm1Dran
Ifngtm1Ts/Ifngtm1Ts
Il3tm1Glli/Il3tm1Glli
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csf2tm1Dran mutation (0 available); any Csf2 mutation (13 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Il3tm1Glli mutation (1 available); any Il3 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• particularly prevalent

reproductive system
• particularly prevalent

mortality/aging
• about 40% of homozygotes died of pneumonia in the first few weeks of life
• surviving mice became moribund with time
• most died or had to be euthanized before 14 months of age

immune system
• mild eosinophilia in mice surviving beyond the first few weeks of life
• serum levels increased but not significantly
• significantly higher serum IgG1 levels
• non significant increases in serum IgG2b levels
• acute and chronic inflammatory reactions found in many organs and tissues

neoplasm
• Lymphoproliferative disease in a high proportion of mice
• develops into B cell lymphomas
• solid tumors are benign to metastasizing carcinomas
• particularly prevalent

hematopoietic system
• mild eosinophilia in mice surviving beyond the first few weeks of life
• serum levels increased but not significantly
• significantly higher serum IgG1 levels
• non significant increases in serum IgG2b levels

Mouse Models of Human Disease
OMIM ID Ref(s)
NOT Systemic Lupus Erythematosus; SLE 152700 J:83086




Genotype
MGI:3783715
cx26
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Socs1tm1Jni/Socs1tm1Jni
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Socs1tm1Jni mutation (0 available); any Socs1 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• following culturing of IL-17 producing T cells in vitro, IL-17 production is twice as high as in similarly treated wild-type cells




Genotype
MGI:5474288
cx27
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Nlrp1aNeut1/Nlrp1aNeut1
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Nlrp1aNeut1 mutation (0 available); any Nlrp1a mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• normal blood neutrophils and survival
• develop encephalitis

nervous system
• develop encephalitis




Genotype
MGI:5688500
cx28
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Tg(SFTPC-Il18)AThos/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6N * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Tg(SFTPC-Il18)AThos mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice exhibit more severe emphysematous changes and pulmonary inflammation with swelled alveolar macrophages than in single transgenic mice

respiratory system
• mice exhibit more severe emphysematous changes and pulmonary inflammation with swelled alveolar macrophages than in single transgenic mice
• the mean alveolar chord length is greater than in wild-type mice and single Tg(SFTPC-Il18)AThos transgenic mice
• mice exhibit more severe emphysematous changes and pulmonary inflammation with swelled alveolar macrophages than in single transgenic mice
• lung volume is higher than in wild-type or single transgenic mice




Genotype
MGI:4839049
cx29
Allelic
Composition
Faslpr/Faslpr
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
involves: 129S7/SvEvBrd * DBA/1 * MRL/Mp
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Faslpr mutation (24 available); any Fas mutation (54 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• decrease in the number of CD4-CD8-B220+ alpha beta T cells compared to mice homozygous for Faslpr and wild-type for Ifng
• lympadenopathy (based on spleen weight and cellularity) is reduced compared to mice homozygous for Faslpr and wild-type for Ifng
• at 7-8 months of age a modest increase in spleen size and cellularity is seen relative to wild-type controls
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• lympadenopathy (based on lymph node weight and cellularity) is reduced compared to mice homozygous for Faslpr and wild-type for Ifng
• in young animals lymph node size is similar to wild-type controls
• at 7-8 months of age a modest increase in lymph node size and cellularity is seen relative to wild-type controls
• while mice develop the typical autoimmune lesions, end organ disease is decreased compared to mice homozygous for Faslpr and wild-type for Ifng
• lower titers of anti-snRNP and anti-rheumatoid factors antibodies relative to mice homozygous for Faslpr and wild-type for Ifng at 3 and 7-8 months of age
• at 3 and 7-8 months of age

homeostasis/metabolism
• levels are lower compared to mice homozygous for Faslpr and wild-type for Ifng

hematopoietic system
• decrease in the number of CD4-CD8-B220+ alpha beta T cells compared to mice homozygous for Faslpr and wild-type for Ifng
• lympadenopathy (based on spleen weight and cellularity) is reduced compared to mice homozygous for Faslpr and wild-type for Ifng
• at 7-8 months of age a modest increase in spleen size and cellularity is seen relative to wild-type controls
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng
• at 3 and 7-8 months of age relative to mice homozygous for Faslpr and wild-type for Ifng




Genotype
MGI:3629594
cx30
Allelic
Composition
Ifngtm1Ts/Ifngtm1Ts
Tnftm2Gkl/Tnf+
Genetic
Background
involves: 129S/SvEv * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
Tnftm2Gkl mutation (1 available); any Tnf mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• development and severity of IBD are similar to Tnftm2Gkl/+, wild-type Ifng controls

digestive/alimentary system
• development and severity of IBD are similar to Tnftm2Gkl/+, wild-type Ifng controls




Genotype
MGI:3801419
cx31
Allelic
Composition
Faslpr/Faslpr
Ifngtm1Ts/Ifng+
Genetic
Background
MRL.Cg-Ifngtm1Ts Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Faslpr mutation (24 available); any Fas mutation (54 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice become moribund and are sacrificed at 4 months mutants posttransfer of Ifng wild-type F4/80+ macrophages at 2 months while all controls remain alive

immune system
• macrophage accumulation is reduced compared to Faslpr homozygotes
• mice develop glomerular autoantibody deposits, but do not develop glomerulonephritis
• mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months develop diffuse proliferative glomerulonephritis by 6 months

renal/urinary system
• glomeruli are hypercellular in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months
• glomerular damage is more severe in mice receiving cell transfer than in control mice not receiving transfers
• thickening of capillary walls in glomeruli is observed in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months
• mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months develop diffuse proliferative glomerulonephritis by 6 months
• mesangial cells are increased in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months

homeostasis/metabolism
• BUN levels are elevated at time of death in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months

cardiovascular system
• thickening of capillary walls in glomeruli is observed in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months

cellular
• macrophage accumulation is reduced compared to Faslpr homozygotes

hematopoietic system
• macrophage accumulation is reduced compared to Faslpr homozygotes




Genotype
MGI:3801418
cx32
Allelic
Composition
Faslpr/Faslpr
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
MRL.Cg-Ifngtm1Ts Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Faslpr mutation (24 available); any Fas mutation (54 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• at 4 months, kidney-infiltrating macrophages are not present; deposits of glomerular immune complexes (ICs) are not observed
• in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages, IC deposition and glomerular proliferation are similar to control mice not receiving transfers
• in mutants receiving adoptive transfer of Ifng wild-type T cells at 2 months, kidney interstitium remains free of macrophages, T cells, or other lymphocytes (signs of kidney interstitial inflammation) at 2 months post-transfer
• in mutants receiving adoptive transfer of Ifng wild-type T cells at 2 months, anti-DNA autoantibody production is minimal compared to Ifng-wild-type, Faslpr homozygotes; glomerular autoantibody deposits are not observed
• macrophage accumulation is reduced compared to Faslpr homozygotes
• in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages, migration of macrophages to peritubular and periglomerular areas of kidneys is detected, whereas without transfer, macrophage recruitment to these areas is significantly reduced relative to Faslpr homozygotes
• mice display perivascular infiltrate composed mainly of CD4+ cells
• mutants receiving adoptive transfer of Ifng wild-type T cells at 2 months develop heavy perivascular infiltrates of mainly CD4+ T cells but show no signs of glomerular nephritis, similar to nontransferred controls
• severe multifocal pyogranulomatous nephritis is observed in kidneys of mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months of age, with extensive perivascular and periglomerular accumulation of polymorphonuclear leukocytes and mononuclear cells
• mutants receiving adoptive transfer of Ifng wild-type T cells at 2 months develop diffuse severe acidophilic pneumonia, characterized by intraalveolar accumulation of strongly eosinophilic macrophages with heavy CD3+ cell infiltration; some animals present with peribronchial T cell infiltration

renal/urinary system
• mice display perivascular infiltrate composed mainly of CD4+ cells
• mutants receiving adoptive transfer of Ifng wild-type T cells at 2 months develop heavy perivascular infiltrates of mainly CD4+ T cells but show no signs of glomerular nephritis, similar to nontransferred controls
• severe multifocal pyogranulomatous nephritis is observed in kidneys of mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages at 2 months of age, with extensive perivascular and periglomerular accumulation of polymorphonuclear leukocytes and mononuclear cells
• in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages, glomerular nephritis is not observed, but severe multifocal pyogranulomatous nephritis in kidneys is observed

respiratory system
• mutants receiving adoptive transfer of Ifng wild-type T cells at 2 months develop diffuse severe acidophilic pneumonia, characterized by intraalveolar accumulation of strongly eosinophilic macrophages with heavy CD3+ cell infiltration; some animals present with peribronchial T cell infiltration

cellular
• macrophage accumulation is reduced compared to Faslpr homozygotes
• in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages, migration of macrophages to peritubular and periglomerular areas of kidneys is detected, whereas without transfer, macrophage recruitment to these areas is significantly reduced relative to Faslpr homozygotes

hematopoietic system
• macrophage accumulation is reduced compared to Faslpr homozygotes
• in mutants receiving adoptive transfer of Ifng wild-type F4/80+ macrophages, migration of macrophages to peritubular and periglomerular areas of kidneys is detected, whereas without transfer, macrophage recruitment to these areas is significantly reduced relative to Faslpr homozygotes





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last database update
06/22/2016
MGI 6.04
The Jackson Laboratory