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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tnfrsf1atm1Blt
targeted mutation 1, Horst Bluethmann
MGI:1861040
Summary 11 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt B6.129P2-Tnfrsf1atm1Blt MGI:3622068
hm2
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt C.129P2-Tnfrsf1atm1Blt MGI:3622067
hm3
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt involves: 129P2/OlaHsd MGI:5573127
hm4
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt involves: 129P2/OlaHsd * C57BL/6 MGI:3622070
hm5
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:4354644
ht6
Tnfrsf1atm1Blt/Tnfrsf1a+ involves: 129P2/OlaHsd MGI:5573128
cn7
Tnfrsf1atm1Blt/Tnfrsf1atm2Gkl
Tg(Cr2-cre)3Cgn/0
involves: 129P2/OlaHsd * 129S/SvEv MGI:3687172
cx8
Ifngtm1Ts/Ifngtm1Ts
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Tnfrsf1btm1Mwm/Tnfrsf1btm1Mwm
involves: 129P2/OlaHsd * 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 MGI:4843969
cx9
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Tnfrsf1btm1Mwm/Tnfrsf1btm1Mwm
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:4838237
cx10
Tnftm2Gkl/Tnftm2Gkl
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 MGI:3622063
cx11
Tg(Gfap-TNF*)K21Gkl/0
Tnfrsf1atm1Blt/Tnfrsf1a+
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:4461138


Genotype
MGI:3622068
hm1
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Genetic
Background
B6.129P2-Tnfrsf1atm1Blt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 7 days after traumatic spinal cord injury increased cell death is seen in the spinal cord compared to wild-type or Tnfrsf1btm1Mwm homozygotes
• 7 days after traumatic spinal cord injury the rostrocaudal spread of the lesion is increased and tissue destruction is more severe compared to wild-type mice
• 4 weeks after traumatic spinal cord injury locomotor performance is significantly more impaired and lesions are longer

behavior/neurological
• after sleep deprivation, mice exhibit increased slow 'slow waves' and negative rebound during the dark period unlike wild-type mice




Genotype
MGI:3622067
hm2
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Genetic
Background
C.129P2-Tnfrsf1atm1Blt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• decreased mortality is seen after exposure to 750 mg acetaminophen /kg

homeostasis/metabolism
• decreased mortality is seen after exposure to 750 mg acetaminophen /kg
• little or no liver damage, reduced infiltration of neutrophils and macrophages into the liver, and reduced intrahepatic chemokine production are seen after exposure to 600 mg acetaminophen /kg




Genotype
MGI:5573127
hm3
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Germinal centers and follicular dendritic cell networks are absent in Tnfrsf1atm1Blt/Tnfrsf1atm1Blt mice immunized with sheep red blood cells

mortality/aging
• all mice infected with Listeria monocytogenes die unlike wild-type mice
• no mice treated with TNF die unlike wild-type mice

immune system
• mice immunized with sheep red blood cells fail to exhibit germinal centers and follicular dendritic cell networks with no antibody response unlike wild-type mice
• all mice infected with Listeria monocytogenes die unlike wild-type mice

homeostasis/metabolism
• TNF-treated mice fail to exhibit lethality, IL6 induction, hypothermia, sickness symptoms (ruffled fur, diarrhea and physical inactivity) or liver and kidney damage unlike wild-type mice

cellular
• in mouse embryonic fibroblasts exposed to hypoxia




Genotype
MGI:3622070
hm4
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• organized follicular dendritic cell networks are absent
• the typical subepithelial dome areas fail to form
• B cells are present but no organized follicles are seen and organized follicular dendritic cell networks are absent
• average of 2 - 4 per mouse compared to 6 - 8 in wild-type mice
• however, T cell populations in the thymus and T and B cell populations in the spleen and lymph nodes are normal
• B cell follicles and follicular dendritic cell network formation are impaired in mesenteric and peripheral lymph nodes; however B cells are present and B and T cell areas are segregated
• following treatment with MOG
• significant reduction in bronchoalveolar lavage leukocytosis in an ovalbumin-induced allergic asthma model
• LPS-induced IL-6 secretion is reduced about 3-fold compared to wild-type mice; however TNF secretion is similar to wild-type
• following treatment with MOG, mice exhibit delayed onset, decreased severity of disease, a 6-fold reduction in demyelination area, and decreased MOG-specific IgG response but increased number of inflammatory foci compared with similarly treated wild-type mice
• infection with as few as 250 colony forming units of Listeria monocytogenes results in 100% mortality by 6 days after infection, all wild-type mice survive this treatment
• D-galactosamine sensitized homozygotes can survive 100-fold higher concentrations of LPS than wild-type; however without D-galactosamine sensitization both types of mice show similar sensitivity to LPS-induced mortality
• however, homozygotes are able to control infections of lymphocytic choriomeningitis virus
• T. gondii-exposed mice exhibit increased bacterial load compared with similarly treated wild-type mice
• however, recruitment and intracerebral cell movement is normal in T. gondii-exposed mice

hematopoietic system
• following treatment with MOG




Genotype
MGI:4354644
hm5
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• following exposure to Pseudomonas aerugiosa exotoxin

immune system
• mice exhibit reduced Pseudomonas aerugiosa exotoxin-induced liver failure compared with similarly treated wild-type mice




Genotype
MGI:5573128
ht6
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1a+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no mice treated with TNF die unlike all wild-type mice

immune system
• decreased induction in TNF-treated mice

homeostasis/metabolism
• decreased induction in TNF-treated mice
• TNF-treated mice fail to exhibit lethality, as great IL6 induction, hypothermia, sickness symptoms (ruffled fur, diarrhea and physical inactivity) or liver and kidney damage unlike wild-type mice




Genotype
MGI:3687172
cn7
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm2Gkl
Tg(Cr2-cre)3Cgn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Cr2-cre)3Cgn mutation (2 available)
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
Tnfrsf1atm2Gkl mutation (1 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• architecture of all secondary lymphoid organs is similar to wild-type




Genotype
MGI:4843969
cx8
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 (23 available)
Tnfrsf1btm1Mwm mutation (2 available); any Tnfrsf1b mutation (16 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:4838237
cx9
Allelic
Composition
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Tnfrsf1btm1Mwm/Tnfrsf1btm1Mwm
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
Tnfrsf1btm1Mwm mutation (2 available); any Tnfrsf1b mutation (16 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
• despite the absence of germinal centers the white pulp has distinct T and B cell areas
• following treatment with MOG
• grossly unidentifiable and histologically hypoplastic
• thin and lack primary and secondary cortical follicles
• following treatment with MOG, mice exhibit delayed onset, decreased severity of disease, a 6-fold reduction in demyelination area, and decreased MOG-specific IgG response but increased number of inflammatory foci compared with similarly treated wild-type mice
• T. gondii-exposed mice exhibit increased bacterial load compared with similarly treated wild-type mice
• however, recruitment and intracerebral cell movement is normal in T. gondii-exposed mice

hematopoietic system
• despite the absence of germinal centers the white pulp has distinct T and B cell areas
• following treatment with MOG




Genotype
MGI:3622063
cx10
Allelic
Composition
Tnftm2Gkl/Tnftm2Gkl
Tnfrsf1atm1Blt/Tnfrsf1atm1Blt
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
Tnftm2Gkl mutation (1 available); any Tnf mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• at 6 weeks of age circulating levels of TNF are 320 +/- 160 pg/ml in disease free mutants compared to undetectable levels in wild-type mice
• however, no signs of arthritis or inflammatory bowel disease are detected
• increased basal and LPS-induced secretion of TNF from thioglycollate-elicited peritoneal macrophages and bone marrow-derived macrophages
• primary synovial and lung fibroblasts display spontaneous TNF secretion and increased secretion following LPS stimulation unlike controls

homeostasis/metabolism
• at 6 weeks of age circulating levels of TNF are 320 +/- 160 pg/ml in disease free mutants compared to undetectable levels in wild-type mice
• however, no signs of arthritis or inflammatory bowel disease are detected




Genotype
MGI:4461138
cx11
Allelic
Composition
Tg(Gfap-TNF*)K21Gkl/0
Tnfrsf1atm1Blt/Tnfrsf1a+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Gfap-TNF*)K21Gkl mutation (1 available)
Tnfrsf1atm1Blt mutation (5 available); any Tnfrsf1a mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• neurological symptoms by the sixth month of age, delayed compared to Tg alone
• at 6 months CNS shows symmetrical, focal demyelinated plaques at the capsula interna and in the spinal cord

Mouse Models of Human Disease
OMIM ID Ref(s)
Multiple Sclerosis, Susceptibility To; MS 126200 J:106592





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last database update
09/27/2016
MGI 6.05
The Jackson Laboratory