Overview

Also Known As:Ifng KO

Macrophages from mice homozygous for the Ifng^tm1Ts knock-out allele show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.

Donating Investigator

Dr. Timothy Stewart

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

Ifng^tm1Ts

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ifng	interferon gamma

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Research Applications

Cancer Research
Hematological Research
Immunology, Inflammation and Autoimmunity Research

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Base Price

Starting at:

$126.51 Domestic price for male 3-week

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Details

Detailed Description

Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.

Development

A targeting vector containing a neo cassette was used to disrupt exon 2. The construct was electroporated into 129S7/SvEvBrd-Hprt1⁺ derived AB1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The resulting mice were backcrossed onto the C57BL/6 background for 8 generations by the donating investigator before arriving at The Jackson Laboratory.

Control Suggestions

Approximate Controls

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Dalton DK; Pitts-Meek S; Keshav S; Figari IS; Bradley A; Stewart TA. 1993. Multiple defects of immune cell function in mice with disrupted interferon-gamma genes [see comments] Science 259(5102):1739-42PubMed: 8456300 MGI: J:66802

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Genetics

Ifng^tm1Ts

Allele Symbol: Ifng^tm1Ts

Allele Name	targeted mutation 1, Timothy Stewart
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	gko; ifg^tm1; Ifn^tm/Ts; ifn^tm1Ts; IFN-g KO; ifng^-; Ifng^tm1Ts; Ifn-g^tm1Ts; IFN-gamma-; IFNgamma-; IFNgamma KO; IFN-gamma KO; IFN-gamma^tm1Ts; IFN-gammaKO; Ifngtm1Ts
Gene Symbol and Name	Ifng, interferon gamma
Gene Synonym(s)
Strain of Origin	129S7/SvEvBrd-Hprt⁺
Chromosome	10
Molecular Note	Insertion of a neomycin gene into exon 2, which introduced a termination codon after the first 30 amino acids of the mature protein.
Mutations Made By	Dr. Timothy Stewart

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

malaria

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Ifng^tm1Ts related

Cancer Research
- Growth Factors/Receptors/Cytokines
Hematological Research
- Immunological Defects
Immunology, Inflammation and Autoimmunity Research
- Growth Factors/Receptors/Cytokines
- Inflammation
- Immunodeficiency
  - multiple immune defects

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * BALB/c

hematopoietic system phenotype

decreased IgE level
- ovalbumin challenge fails to significantly potentiate ovalbumin specific IgE levels, unlike in wild-type controls

immune system phenotype

decreased IgE level
- ovalbumin challenge fails to significantly potentiate ovalbumin specific IgE levels, unlike in wild-type controls

decreased inflammatory response
- the eosinophilic response in ovalbumin challenged mice is reduced compared to wild-type controls

abnormal susceptibility to infection
- Normal - 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
- mice are able to clear infectious Murine gammaherpesvirus 68 (MHV-68) from their lungs but with a slight delay relative wild-type mice

mammalian phenotype

immune system phenotype
- Normal - 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

respiratory system phenotype

decreased airway responsiveness
- ovalbumin challenge fails to induce airway hyperresponsiveness unlike in wild-type mice

increased airway responsiveness
- in saline challenged mice relative to wild-type controls

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
C.129S7(B6)-Ifng/J

growth/size/body region phenotype

enlarged spleen
- develop splenomegaly after infection with BCG

hematopoietic system phenotype

abnormal spleen white pulp morphology
- 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

pale spleen
- spleens become paler as BCG infection proceeds

abnormal uterine NK cell physiology
- 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

extramedullary hematopoiesis
- following infection with BCG

abnormal NK cell physiology
- decrease in the cytotoxicity of NK cells from mice primed with rIL12

abnormal spleen morphology

abnormal spleen red pulp morphology
- 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

abnormal uterine NK cell morphology
- 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

enlarged spleen
- develop splenomegaly after infection with BCG

increased leukocyte cell number
- following infection with BCG

abnormal macrophage physiology
- exposure to rIL12 fails to prime macrophages against subsequent LPS exposure

abnormal cytotoxic T cell physiology
- C26 cells induce slightly reduced CTL activity compared to the response in similarly treat wild-type mice

increased uterine NK cell number
- after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls

increased granulocyte number
- in the blood, bone marrow and spleen following infection with BCG

increased monocyte cell number
- following infection with BCG

homeostasis/metabolism phenotype

abnormal circulating cytokine level
- increase in circulating levels of CSF3 after infection with BCG especially in moribund mice

increased circulating interleukin-6 level
- following infection with BCG

immune system phenotype

abnormal adaptive immunity

abnormal spleen morphology

abnormal uterine NK cell morphology
- 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

increased leukocyte cell number
- following infection with BCG

increased susceptibility to bacterial infection induced morbidity/mortality
- die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis

abnormal spleen white pulp morphology
- 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

abnormal uterine NK cell physiology
- 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

increased susceptibility to bacterial infection
- following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen
- 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

increased circulating interleukin-6 level
- following infection with BCG

abnormal NK cell physiology
- decrease in the cytotoxicity of NK cells from mice primed with rIL12

abnormal cytotoxic T cell physiology
- C26 cells induce slightly reduced CTL activity compared to the response in similarly treat wild-type mice

abnormal macrophage physiology
- exposure to rIL12 fails to prime macrophages against subsequent LPS exposure

abnormal spleen red pulp morphology
- 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

decreased susceptibility to parasitic infection
- 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

increased uterine NK cell number
- after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls

pale spleen
- spleens become paler as BCG infection proceeds

increased monocyte cell number
- following infection with BCG

abnormal circulating cytokine level
- increase in circulating levels of CSF3 after infection with BCG especially in moribund mice

abnormal cytokine secretion
- lymphocytes form C25/Il12 cell primed mice produce about 3 fold higher levels of CSF2

abnormal inflammatory response
- 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

enlarged spleen
- develop splenomegaly after infection with BCG

increased granulocyte number
- in the blood, bone marrow and spleen following infection with BCG

behavior/neurological phenotype

increased fear-related response
- 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
- prolonged freeze time following a startle stimulus relative to wild-type controls

abnormal response to new 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
- the number of rearings is decreased in a novel environment

decreased vertical activity
- in a novel environment

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis

neoplasm

abnormal tumor pathology
- 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

decreased tumor latency
- Normal - however, no difference is detected when parental C26 cells are used
- 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

reproductive system phenotype

abnormal uterine NK cell physiology
- uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
- decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation

decreased litter size
- phenotype is independent of the genotype of the embryos
- Normal - no difference in litter size or number of resorbed embryos is detected in subsequent pregnancies
- decrease in litter size and increase in the number of resorbed embryos in the first litter

increased uterine NK cell number
- after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls

abnormal uterine NK cell morphology
- 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

abnormal maternal decidual layer morphology
- 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

embryo phenotype

increased uterine NK cell number
- after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls

abnormal maternal decidual layer morphology
- 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

abnormal uterine NK cell morphology
- 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

endocrine/exocrine gland phenotype

abnormal uterine NK cell morphology
- 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

increased uterine NK cell number
- after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * C57BL/6

cellular phenotype

increased splenocyte proliferation
- splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

immune system phenotype

abnormal macrophage physiology
- macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge
- macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge

abnormal NK cell physiology
- significantly lower resting splenic NK cell activity
- Normal - however, the recruitment of T cells by IL12 is not impaired
- recruitment of NK cells to the liver by recombinant murine IL12 is impaired

decreased susceptibility to parasitic infection
- mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice
- Normal - however, IFNG-competent alpha+CD4+ T cells promote experimental cerebral malaria

abnormal type IV hypersensitivity reaction
- Normal - however, the type IV hypersensitivity reaction in the absence of UV exposure is similar to controls
- exposure to UVA and UVB fails to significantly reduce the UVB induced suppression of the type IV hypersensitivity reaction

abnormal MHC II cell surface expression on macrophages
- macrophages from BCG infected mice exhibit reduced class II expression

decreased length of allograft survival
- reduced surival of cardiac grafts relative to controls

decreased susceptibility to parasitic infection induced morbidity/mortality
- mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice

increased splenocyte proliferation
- splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

increased susceptibility to bacterial infection
- increased mortality following a sublethal dose of Mycobacterium bovis (BCG )

craniofacial phenotype

alveolar process atrophy
- modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

integument phenotype

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

growth/size/body region phenotype

alveolar process atrophy
- modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

mammalian phenotype

immune system phenotype
- Normal - mice are able to clear infections of Pneumocystis carinii, similar to controls

mortality/aging

decreased susceptibility to parasitic infection induced morbidity/mortality
- mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice

neoplasm

increased metastatic potential
- 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

decreased tumor incidence
- tumor-bearing mice treated with Th-17-polarized cells from Tg(Tcra,Tcrb)9Rest cells show increased tumor rejection compared to controls

skeleton phenotype

alveolar process atrophy
- modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

hematopoietic system phenotype

abnormal macrophage physiology
- macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge
- macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge

abnormal NK cell physiology
- Normal - however, the recruitment of T cells by IL12 is not impaired
- recruitment of NK cells to the liver by recombinant murine IL12 is impaired
- significantly lower resting splenic NK cell activity

increased splenocyte proliferation
- splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

abnormal MHC II cell surface expression on macrophages
- macrophages from BCG infected mice exhibit reduced class II expression

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * A/WySn * C57BL/10SnSg * Swiss

hematopoietic system phenotype

increased IgG1 level
- relative to wild-type controls
- however, mercury treatment does not result in an increase in IgG1 levels

decreased IgG2a level
- following exposure to HgCl2 for 4 weeks, relative to similarly treated wild-type and heterozygous mice

decreased IgG level
- decrease in the induction of IgG in response to low levels of antigen ((4-hydroxy-3 nitrophenyl)acetyl)

homeostasis/metabolism phenotype

decreased physiological sensitivity to xenobiotic
- resistant to mercury induced autoimmune response

immune system phenotype

decreased susceptibility to autoimmune disorder
- resistant to mercury induced autoimmune response

increased IgG1 level
- relative to wild-type controls
- however, mercury treatment does not result in an increase in IgG1 levels

decreased IgG2a level
- following exposure to HgCl2 for 4 weeks, relative to similarly treated wild-type and heterozygous mice

decreased IgG level
- decrease in the induction of IgG in response to low levels of antigen ((4-hydroxy-3 nitrophenyl)acetyl)

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd

cardiovascular system phenotype

corneal vascularization
- 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 phenotype

abnormal immunoglobulin level
- 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

impaired natural killer cell mediated cytotoxicity
- activated splenic and liver NK cells are less efficient in their killing of 4T1 or Renca tumor target cells

increased IgG1 level
- following infection with type A influenza

mortality/aging

increased susceptibility to Herpesvirales infection induced morbidity/mortality
- 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

increased susceptibility to bacterial infection induced morbidity/mortality
- treatment with exogenous IFNG improves survival
- mean survival time following infecting with virulent Mycobacterium tuberculosis is 15 days compared to over 60 days for wild-type controls

increased susceptibility to viral infection induced morbidity/mortality
- 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 phenotype

corneal vascularization
- 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 phenotype

abnormal cytokine level
- 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

immune system phenotype

abnormal immunoglobulin level
- 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

abnormal response to infection
- the magnitude of the delayed type hypersensitive response in mice after HSV-1 infection is reduced compared to BALB/c wild-type controls
- display an increased IgG1 antibody response to type A influenza infection

impaired natural killer cell mediated cytotoxicity
- activated splenic and liver NK cells are less efficient in their killing of 4T1 or Renca tumor target cells

increased susceptibility to bacterial infection
- treatment with exogenous IFNG decreases the bacterial load
- 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

increased susceptibility to Herpesvirales infection
- 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
- 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

abnormal cytokine level
- 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

decreased susceptibility to type IV hypersensitivity reaction
- the magnitude of the delayed type hypersensitive response in mice after HSV-1 infection is reduced compared to BALB/c wild-type controls

increased susceptibility to bacterial infection induced morbidity/mortality
- treatment with exogenous IFNG improves survival
- mean survival time following infecting with virulent Mycobacterium tuberculosis is 15 days compared to over 60 days for wild-type controls

increased susceptibility to Herpesvirales infection induced morbidity/mortality
- 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

increased IgG1 level
- following infection with type A influenza

increased interleukin-17 secretion
- following culturing of IL-17 producing T cells in vitro, IL-17 production is twice as high as in similarly treated wild-type cells

increased susceptibility to viral infection
- 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
- 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

increased susceptibility to viral infection induced morbidity/mortality
- 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

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
C.129S7-Ifng

hematopoietic system phenotype

abnormal immunoglobulin level
- IgG responses are restricted to IgG1 and IgG2b

mammalian phenotype

neoplasm
- Background Sensitivity - unlike mice on a congenic C57BL/6 background, mice on a BALB/c background do not develop disseminated lymphomas

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- Normal - following vaccination mice are able to develop resistance to L. monocytogenes infection
- Normal - however the LD50 for a mutant strain of L. monocytogenes (DP-L1942) is similar in homozygous mice and controls
- the LD50 for Listeria monocytogenes infection is 10 CFU compared to greater than 10⁴ CFU for wild-type and heterozygous controls

increased susceptibility to parasitic infection induced morbidity/mortality
- 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

increased lung adenocarcinoma incidence
- all are well differentiated papillary adenocarcinomas
- in a few mice, with a very late onset

increased tumor latency
- Background Sensitivity - in mice on a BALB/c background compared to mice on a C57BL/6 background

respiratory system phenotype

increased lung adenocarcinoma incidence
- in a few mice, with a very late onset
- all are well differentiated papillary adenocarcinomas

immune system phenotype

abnormal response to infection
- following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice

abnormal humoral immune response
- however, following oral OVA exposure OVA antibody levels are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels
- the magnitude of the OVA specific antibody is reduced
- Normal - following oral OVA exposure OVA antibody levels are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels

increased interleukin-5 secretion
- following infection with T. gondii (irradiate RH strain) splenocytes produce more IL-5 compared to similar cultures from wild-type mice

increased susceptibility to bacterial infection induced morbidity/mortality
- Normal - however the LD50 for a mutant strain of L. monocytogenes (DP-L1942) is similar in homozygous mice and controls
- the LD50 for Listeria monocytogenes infection is 10 CFU compared to greater than 10⁴ CFU for wild-type and heterozygous controls
- Normal - following vaccination mice are able to develop resistance to L. monocytogenes infection

increased susceptibility to experimental autoimmune encephalomyelitis
- immunized mice display meningeal and perivascular inflammatory infiltrates in the spinal cord and brain similar to those seen in susceptible strains like SJL/J
- 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

abnormal cytokine secretion
- following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice

abnormal immunoglobulin level
- IgG responses are restricted to IgG1 and IgG2b

abnormal immune tolerance
- oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent exposure to the same antigen

increased susceptibility to parasitic infection
- 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
- dramatic increase in the number of infected cells expansion of the tissues infected following inoculation with Toxoplasma gondii (strain ME49)
- Normal - IL-2 production in response to infection is similar to controls

increased susceptibility to parasitic infection induced morbidity/mortality
- 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

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * C57BL/6J

immune system phenotype

increased susceptibility to bacterial infection induced morbidity/mortality
- after infection with a normally sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice become severely ill and need to be euthanized

increased susceptibility to bacterial infection
- 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
- 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

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- 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: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * NOD

mammalian phenotype

immune system phenotype
- Background Sensitivity - at generation N4 no difference is seen in the time course of diabetes development in females unlike in mice at generation N7

The following phenotype relates to a compound genotype created using this strain

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
B6.129S7-Ifng

endocrine/exocrine gland phenotype

increased T cell derived lymphoma incidence
- in a few mice

immune system phenotype

abnormal immunoglobulin level

abnormal cytokine secretion
- following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
- after infection with Leishmania major the number of lymphocytes producing IL4 increases unlike in control mice where the number of lymphocytes producing IFNG increases

abnormal response to infection
- after infection with Leishmania major levels of IgG1 and IgE are increased while levels of IgG2a and IgG3 remain low
- after infection with Leishmania major mice display minimal Th1 type responses and increased Th2 type responses
- following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice

increased IgG1 level
- 5-fold increase in the serum levels of JHMV specific IgG1 at 14 days post infection compared to infected wild-type controls
- after infection with Leishmania major

increased susceptibility to viral infection induced morbidity/mortality
- higher mortality is seen following infection with JHMV compared to wild-type controls

increased interleukin-10 secretion
- 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

increased susceptibility to parasitic infection induced morbidity/mortality
- sudden death occurs 5 to 7 weeks after infection with Leishmania major
- die earlier after inoculation with Toxoplasma gondii (strain ME49) compared to wild-type controls

increased susceptibility to Coronaviridae infection
- 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
- 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
- Normal - however, no differences are found in JHMV specific cytotoxic T lymphocyte activity

increased susceptibility to viral infection
- Normal - 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
- 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

increased interleukin-2 secretion
- 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

abnormal response to transplant
- after immunosuppressive treatment (anti-CD4 and anti-CD8 mAbs) allografts (BALB/c, H2-Ab1^bm12 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
- s of rejection but develop coronary arteriopathy

decreased IgG3 level
- after infection with Leishmania major

increased IgE level
- after infection with Leishmania major

increased interleukin-5 secretion
- 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

increased susceptibility to parasitic infection
- 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

abnormal lymph node cell ratio
- significant increase in the numbers of immature B cells in the lymph nodes

decreased IgG2a level
- after infection with Leishmania major

increased CD8-positive, alpha-beta T cell number
- 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

abnormal B cell physiology
- immature B cells fail to be excluded from the lymph nodes

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- higher mortality is seen following infection with JHMV compared to wild-type controls

hematopoietic system phenotype

decreased IgG2a level
- after infection with Leishmania major

decreased IgG3 level
- after infection with Leishmania major

increased CD8-positive, alpha-beta T cell number
- 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

abnormal immunoglobulin level

increased IgG1 level
- 5-fold increase in the serum levels of JHMV specific IgG1 at 14 days post infection compared to infected wild-type controls
- after infection with Leishmania major

abnormal B cell physiology
- immature B cells fail to be excluded from the lymph nodes

increased IgE level
- after infection with Leishmania major

mortality/aging

increased susceptibility to viral infection induced morbidity/mortality
- higher mortality is seen following infection with JHMV compared to wild-type controls

increased susceptibility to parasitic infection induced morbidity/mortality
- die earlier after inoculation with Toxoplasma gondii (strain ME49) compared to wild-type controls
- sudden death occurs 5 to 7 weeks after infection with Leishmania major

premature death
- Background Sensitivity - in mice on a C57BL/6 background compared to mice on a BALB/c background

increased susceptibility to Coronaviridae infection induced morbidity/mortality
- higher mortality is seen following infection with JHMV compared to wild-type controls

neoplasm

decreased tumor latency
- Background Sensitivity - in mice on a C57BL/6 background compared to mice on a BALB/c background

increased lymphoma incidence
- most lymphomas are diffuse large cell lymphomas
- 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

increased sarcoma incidence
- in a few mice

increased T cell derived lymphoma incidence
- in a few mice

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
B6.129S7-Ifng/J

digestive/alimentary phenotype

stomach inflammation
- 5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice

growth/size/body region phenotype

enlarged spleen
- develop splenomegaly after infection with BCG

hematopoietic system phenotype

abnormal macrophage chemotaxis
- 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice

extramedullary hematopoiesis
- following infection with BCG

abnormal immunoglobulin level
- IgG responses are restricted to IgG1 and IgG2b

abnormal spleen white pulp morphology
- 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

increased NK T cell number
- unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers

enlarged spleen
- develop splenomegaly after infection with BCG

increased granulocyte number
- in the blood, bone marrow and spleen following infection with BCG

abnormal dendritic cell chemotaxis
- enhancement in LPS induced dendritic cell migration to the spleen
- enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro

abnormal spleen morphology

increased leukocyte cell number
- following infection with BCG

increased monocyte cell number
- following infection with BCG

pale spleen
- spleens become paler as BCG infection proceeds

abnormal spleen red pulp morphology
- 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

homeostasis/metabolism phenotype

abnormal circulating cytokine level
- increase in circulating levels of CSF3 after infection with BCG especially in moribund mice

abnormal urine homeostasis
- 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

abnormal response to 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
- decrease in the number and area of regenerating muscle fibers 5 and 10 days after muscle injury

decreased susceptibility to injury
- 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
- Normal - however, after 84 h of exposure to hyperoxia these measures are not different from similarly exposed to wild-type controls

abnormal nitric oxide homeostasis
- unlike in wild-type mice, treatment with LPS and DGalN fails to increase nitric oxide levels

increased circulating interleukin-6 level
- following infection with BCG

albuminuria
- increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis

increased sensitivity to xenobiotic induced morbidity/mortality
- increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls

behavior/neurological phenotype

abnormal response to new environment
- 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 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

decreased vertical activity
- in a novel environment

increased fear-related response
- make fewer entries and spend less time in the open arms of an elevated maze relative to wild-type controls
- prolonged freeze time and longer time to return to normal open field activity patterns following a startle stimulus relative to wild-type 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

immune system phenotype

abnormal dendritic cell chemotaxis
- 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

abnormal dendritic cell physiology
- increase in IL12 and decrease in IL10 secretion following LPS stimulation

abnormal spleen white pulp morphology
- 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

increased circulating interleukin-6 level
- following infection with BCG

abnormal dendritic cell antigen presentation
- dendritic cells show a greater ability to stimulate T cell proliferation in vitro

abnormal immune tolerance
- oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent subcutaneous exposure to the same antigen

decreased interleukin-10 secretion
- by bone marrow dendritic cells following LPS stimulation
- splenocytes from Helicobacter pylori infected mice produce 4-fold less IL-10 when cultured in the presence of H. pylori antigen

abnormal macrophage chemotaxis
- 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice

enlarged spleen
- develop splenomegaly after infection with BCG

increased leukocyte cell number
- following infection with BCG

increased susceptibility to parasitic infection
- Background Sensitivity - d in about 50% of mice gallbladders are enlarged
- 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
- 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

increased monocyte cell number
- following infection with BCG

increased NK T cell number
- unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers

increased susceptibility to bacterial infection
- following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen
- 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

decreased interferon-gamma secretion
- splenocytes fail to produce IFN-gamma in response to H. pylori antigen stimulation

pale spleen
- spleens become paler as BCG infection proceeds

abnormal cytokine secretion

abnormal circulating cytokine level
- increase in circulating levels of CSF3 after infection with BCG especially in moribund mice

decreased length of allograft survival
- 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

glomerulonephritis
- increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes

increased interleukin-4 secretion
- 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

abnormal Langerhans cell physiology
- enhancement in hapten induced Langerhan cell migration to the draining lymph nodes

abnormal spleen red pulp morphology
- 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

abnormal type IV hypersensitivity reaction
- 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

enlarged mesenteric lymph nodes
- in C. parvum infected mice

increased granulocyte number
- in the blood, bone marrow and spleen following infection with BCG

increased interleukin-12 secretion
- by bone marrow dendritic cells following LPS stimulation

increased susceptibility to bacterial infection induced morbidity/mortality
- die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis

increased susceptibility to parasitic infection induced morbidity/mortality
- most mice die by 9 days after infection with 1x10⁶ Cryptosporidium parvum oocysts

increased susceptibility to type IV hypersensitivity reaction
- display a more severe delayed type hypersensitivity reaction in response to sheep IgG

abnormal humoral immune response
- 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
- the magnitude of the OVA specific antibody response to subcutaneous OVA challenge is reduced

abnormal immunoglobulin level
- IgG responses are restricted to IgG1 and IgG2b

abnormal spleen morphology

stomach inflammation
- 5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice

mammalian phenotype

immune system phenotype
- Normal - do not exhibit defects on either IgE isotype switch or IgE production

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis

increased susceptibility to parasitic infection induced morbidity/mortality
- most mice die by 9 days after infection with 1x10⁶ Cryptosporidium parvum oocysts

increased sensitivity to xenobiotic induced morbidity/mortality
- increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls

muscle phenotype

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

skeletal muscle fibrosis
- fibrotic lesions are sometimes seen after injury

renal/urinary system phenotype

abnormal urine homeostasis
- 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

glomerulonephritis
- increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes

albuminuria
- increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis

cellular phenotype

abnormal dendritic cell chemotaxis
- 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

abnormal redox activity
- 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

abnormal macrophage chemotaxis
- 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice

References

Dalton DK; Pitts-Meek S; Keshav S; Figari IS; Bradley A; Stewart TA. 1993. Multiple defects of immune cell function in mice with disrupted interferon-gamma genes [see comments] Science 259(5102):1739-42PubMed: 8456300 MGI: J:66802

Additional References

Alcaide P; Fresno M. 2004. The Trypanosoma cruzi membrane mucin AgC10 inhibits T cell activation and IL-2 transcription through L-selectin. Int Immunol 16(10):1365-75PubMed: 15314038 MGI: J:93640
Amiri P; Haak-Frendscho M; Robbins K; McKerrow JH; Stewart T; Jardieu P. 1994. Anti-immunoglobulin E treatment decreases worm burden and egg production in Schistosoma mansoni-infected normal and interferon gamma knockout mice. J Exp Med 180(1):43-51PubMed: 8006599 MGI: J:18740
Arantes RM; Marche HH; Bahia MT; Cunha FQ; Rossi MA; Silva JS. 2004. Interferon-gamma-induced nitric oxide causes intrinsic intestinal denervation in Trypanosoma cruzi-infected mice. Am J Pathol 164(4):1361-8PubMed: 15039223 MGI: J:89108
Bullen DV; Darwiche R; Metcalf D; Handman E; Alexander WS. 2001. Neutralization of interferon-gamma in neonatal SOCS1-/- mice prevents fatty degeneration of the liver but not subsequent fatal inflammatory disease. Immunology 104(1):92-8PubMed: 11576226 MGI: J:71691
Campos MA; Closel M; Valente EP; Cardoso JE; Akira S; Alvarez-Leite JI; Ropert C; Gazzinelli RT. 2004. Impaired production of proinflammatory cytokines and host resistance to acute infection with Trypanosoma cruzi in mice lacking functional myeloid differentiation factor 88. J Immunol 172(3):1711-8PubMed: 14734753 MGI: J:87693
Chan WC; Duong TT; Yeung RS. 2004. Presence of IFN-gamma does not indicate its necessity for induction of coronary arteritis in an animal model of Kawasaki disease. J Immunol 173(5):3492-503PubMed: 15322214 MGI: J:92708
Christensen JE; Wodarz D; Christensen JP; Thomsen AR. 2004. Perforin and IFN-gamma do not significantly regulate the virus-specific CD8+ T cell response in the absence of antiviral effector activity. Eur J Immunol 34(5):1389-94PubMed: 15114672 MGI: J:89390
Cooper AM; Dalton DK; Stewart TA; Griffin JP; Russell DG; Orme IM. 1993. Disseminated tuberculosis in interferon gamma gene-disrupted mice. J Exp Med 178(6):2243-7PubMed: 8245795 MGI: J:15723
Dohi T; Fujihashi K; Kiyono H; Elson CO; McGhee JR. 2000. Mice deficient in Th1- and Th2-type cytokines develop distinct forms of hapten-induced colitis. Gastroenterology 119(3):724-33PubMed: 10982767 MGI: J:64230
Feng CG; Collazo-Custodio CM; Eckhaus M; Hieny S; Belkaid Y; Elkins K; Jankovic D; Taylor GA; Sher A. 2004. Mice deficient in LRG-47 display increased susceptibility to mycobacterial infection associated with the induction of lymphopenia. J Immunol 172(2):1163-8PubMed: 14707092 MGI: J:87364
Fujigaki S; Saito K; Sekikawa K; Tone S; Takikawa O; Fujii H; Wada H; Noma A; Seishima M. 2001. Lipopolysaccharide induction of indoleamine 2,3-dioxygenase is mediated dominantly by an IFN-gamma-independent mechanism. Eur J Immunol 31(8):2313-8PubMed: 11477543 MGI: J:71158
Hanada T; Yoshida H; Kato S; Tanaka K; Masutani K; Tsukada J; Nomura Y; Mimata H; Kubo M; Yoshimura A. 2003. Suppressor of cytokine signaling-1 is essential for suppressing dendritic cell activation and systemic autoimmunity. Immunity 19(3):437-50PubMed: 14499118 MGI: J:85811
Hu C; Mayadas-Norton T; Tanaka K; Chan J; Salgame P. 2000. Mycobacterium tuberculosis infection in complement receptor 3-deficient mice. J Immunol 165(5):2596-602PubMed: 10946287 MGI: J:64055
Kemp RA; Ronchese F. 2001. Tumor-specific tc1, but not tc2, cells deliver protective antitumor immunity. J Immunol 167(11):6497-502PubMed: 11714817 MGI: J:72797
Lambert SL; Okada CY; Levy R. 2004. TCR vaccines against a murine T cell lymphoma: a primary role for antibodies of the IgG2c class in tumor protection. J Immunol 172(2):929-36PubMed: 14707065 MGI: J:87361
Metcalf D; Alexander WS; Ryan PJ; Mifsud S; Di Rago L. 2001. Production of colony-stimulating factors and il-5 by organs from three types of mice with inflammatory disease due to loss of the suppressor of cytokine signaling-1. J Immunol 167(8):4661-7PubMed: 11591796 MGI: J:72058
Murphy EA; Sathiyaseelan J; Parent MA; Zou B; Baldwin CL. 2001. Interferon-gamma is crucial for surviving a Brucella abortus infection in both resistant C57BL/6 and susceptible BALB/c mice. Immunology 103(4):511-8PubMed: 11529943 MGI: J:71148
Murray HW; Lu CM; Brooks EB; Fichtl RE; DeVecchio JL; Heinzel FP. 2003. Modulation of T-cell costimulation as immunotherapy or immunochemotherapy in experimental visceral leishmaniasis. Infect Immun 71(11):6453-62PubMed: 14573667 MGI: J:86275
Nance S; Cross R; Fitzpatrick E. 2004. Chemokine production during hypersensitivity pneumonitis. Eur J Immunol 34(3):677-85PubMed: 14991597 MGI: J:88361
Nansen A; Marker O; Bartholdy C; Thomsen AR. 2000. CCR2+ and CCR5+ CD8+ T cells increase during viral infection and migrate to sites of infection. Eur J Immunol 30(7):1797-806PubMed: 10940868 MGI: J:63499
Nguyen HH; van Ginkel FW; Vu HL; Novak MJ; McGhee JR; Mestecky J. 2000. Gamma interferon is not required for mucosal cytotoxic T-lymphocyte responses or heterosubtypic immunity to influenza A virus infection in mice. J Virol 74(12):5495-501PubMed: 10823854 MGI: J:62303
Okamoto M; Kato S; Oizumi K; Kinoshita M; Inoue Y; Hoshino K; Akira S; McKenzie AN; Young HA; Hoshino T. 2002. Interleukin 18 (IL-18) in synergy with IL-2 induces lethal lung injury in mice: a potential role for cytokines, chemokines, and natural killer cells in the pathogenesis of interstitial pneumonia. Blood 99(4):1289-98PubMed: 11830478 MGI: J:74714
Ponomarev ED; Novikova M; Yassai M; Szczepanik M; Gorski J; Dittel BN. 2004. Gamma delta T cell regulation of IFN-gamma production by central nervous system-infiltrating encephalitogenic T cells: correlation with recovery from experimental autoimmune encephalomyelitis. J Immunol 173(3):1587-95PubMed: 15265886 MGI: J:92038
Scott MJ; Hoth JJ; Stagner MK; Gardner SA; Peyton JC; Cheadle WG. 2004. CD40-CD154 interactions between macrophages and natural killer cells during sepsis are critical for macrophage activation and are not interferon gamma dependent. Clin Exp Immunol 137(3):469-77PubMed: 15320895 MGI: J:92312
Siegmund B; Sennello JA; Lehr HA; Senaldi G; Dinarello CA; Fantuzzi G. 2004. Frontline: Interferon regulatory factor-1 as a protective gene in intestinal inflammation: role of TCR gamma delta T cells and interleukin-18-binding protein. Eur J Immunol 34(9):2356-64PubMed: 15307168 MGI: J:91767
Smith LM; Bonafonte MT; Mead JR. 2000. Cytokine expression and specific lymphocyte proliferation in two strains of Cryptosporidium parvum-infected gamma-interferon knockout mice. J Parasitol 86(2):300-7PubMed: 10780549 MGI: J:62349
Townsend MJ; Weinmann AS; Matsuda JL; Salomon R; Farnham PJ; Biron CA; Gapin L; Glimcher LH. 2004. T-bet regulates the terminal maturation and homeostasis of NK and Valpha14i NKT cells. Immunity 20(4):477-94PubMed: 15084276 MGI: J:89776
Van Uden JH; Tran CH; Carson DA; Raz E. 2001. Type I interferon is required to mount an adaptive response to immunostimulatory DNA. Eur J Immunol 31(11):3281-90PubMed: 11745345 MGI: J:72586
Wilson ME; Recker TJ; Rodriguez NE; Young BM; Burnell KK; Streit JA; Kline JN. 2002. The TGF-beta response to Leishmania chagasi in the absence of IL-12. Eur J Immunol 32(12):3556-65PubMed: 12516540 MGI: J:80857

Additional - Ifng^tm1Ts related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Ifng
- Standard PCR:Ifng
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a good breeder.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Appearance
- black
  Related Genotype: a/a
Citation
When using the Ifng KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #002287 in your Materials and Methods section.

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RB16 (Maximum)

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:Ifng KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Ifngtm1Ts

Allele Symbol: Ifngtm1Ts

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Ifngtm1Ts related

Mammalian Phenotype Terms by Genotype

Genotype: Ifngtm1Ts/Ifngtm1Tsinvolves: 129S7/SvEvBrd * BALB/c

hematopoietic system phenotype

immune system phenotype

mammalian phenotype

respiratory system phenotype

Genotype: Ifngtm1Ts/Ifngtm1TsC.129S7(B6)-Ifng/J

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

behavior/neurological phenotype

mortality/aging

neoplasm

reproductive system phenotype

embryo phenotype

endocrine/exocrine gland phenotype

Genotype: Ifngtm1Ts/Ifngtm1Tsinvolves: 129S7/SvEvBrd * C57BL/6

cellular phenotype

immune system phenotype

craniofacial phenotype

integument phenotype

growth/size/body region phenotype

mammalian phenotype

mortality/aging

neoplasm

skeleton phenotype

hematopoietic system phenotype

Genotype: Ifngtm1Ts/Ifngtm1Tsinvolves: 129S7/SvEvBrd * A/WySn * C57BL/10SnSg * Swiss

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Ifngtm1Ts/Ifngtm1Tsinvolves: 129S7/SvEvBrd

cardiovascular system phenotype

hematopoietic system phenotype

mortality/aging

vision/eye phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Ifngtm1Ts/Ifngtm1TsC.129S7-Ifng

hematopoietic system phenotype

mammalian phenotype

mortality/aging

neoplasm

respiratory system phenotype

immune system phenotype

Genotype: Ifngtm1Ts/Ifngtm1Tsinvolves: 129S7/SvEvBrd * C57BL/6J

immune system phenotype

mortality/aging

Genotype: Ifngtm1Ts/Ifngtm1Tsinvolves: 129S7/SvEvBrd * NOD

mammalian phenotype

Genotype: Ifngtm1Ts/Ifngtm1TsB6.129S7-Ifng

endocrine/exocrine gland phenotype

immune system phenotype

hematopoietic system phenotype

mortality/aging

neoplasm

Genotype: Ifngtm1Ts/Ifngtm1TsB6.129S7-Ifng/J

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

Ifng^tm1Ts

Allele Symbol: Ifng^tm1Ts

Genotype: Ifng^tm1Ts related

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * BALB/c

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
C.129S7(B6)-Ifng/J

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * C57BL/6

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * A/WySn * C57BL/10SnSg * Swiss

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
C.129S7-Ifng

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * C57BL/6J

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
involves: 129S7/SvEvBrd * NOD

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
B6.129S7-Ifng

Genotype: Ifng^tm1Ts/Ifng^tm1Ts
B6.129S7-Ifng/J

Additional - Ifng^tm1Ts related