All Phenotypes Fcer1g<tm1Tks> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Fcer1g^tm1Tks/Fcer1g^tm1Tks	C57BL/6-Fcer1g^tm1Tks	MGI:4360275
hm2	Fcer1g^tm1Tks/Fcer1g^tm1Tks	involves: C57BL/6	MGI:4360109
hm3	Fcer1g^tm1Tks/Fcer1g^tm1Tks	involves: C57BL/6J	MGI:5528882
cx4	Fas^lpr/Fas^lpr Fcer1g^tm1Tks/Fcer1g^tm1Tks	MRL.Cg-Fcer1g^tm1Tks Fas^lpr	MGI:4360203

Allelic Composition	Fcer1g^tm1Tks/Fcer1g^tm1Tks
Genetic Background	C57BL/6-Fcer1g^tm1Tks

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fcer1g^tm1Tks mutation (1 available); any Fcer1g mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

decreased susceptibility to autoimmune hemolytic anemia ( J:145432 )

• mice are resistant to hemolytic anemia induced by self-binding IgG2a antibodies

• no protection is seen with pathogenic self-binding IgA antibodies

hematopoietic system

decreased susceptibility to autoimmune hemolytic anemia ( J:145432 )

• mice are resistant to hemolytic anemia induced by self-binding IgG2a antibodies

• no protection is seen with pathogenic self-binding IgA antibodies

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

decreased T cell proliferation ( J:112160 )

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

impaired macrophage phagocytosis ( J:50023 )

• macrophages have lost the ability to ingest target cells coated in IgG

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:50023 )

• mice are resistant to an induced glumoronephritis disease caused by administration of anti-glomerular basement membrane antibodies (anti-GBM Ab)

• wild-type controls are dead by 14 days after administration while all of the mutant mice survive

homeostasis/metabolism

abnormal cytokine level ( J:258645 )

• production of the cytokines/chemokines monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2) and IL-6 upon stimulation with acylated phosphatidyl-inositol mannosides is lower in peritoneal exudate cells

immune system

decreased T cell proliferation ( J:112160 )

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

decreased IgG level ( J:112160 )

decreased IgG1 level ( J:112160 )

• mice have lower titers of antigen-specific IgG1 2 weeks after immunization compared to controls

decreased IgG2a level ( J:112160 )

• mice have lower titers of antigen-specific IgG2a 2 weeks after immunization compared to controls

decreased IgG2b level ( J:112160 )

• mice have lower titers of antigen-specific IgG2b 2 weeks after immunization compared to controls

decreased IgG3 level ( J:112160 )

• mice have lower titers of antigen-specific IgG3 2 weeks after immunization compared to controls

abnormal NK cell physiology ( J:111365 )

• NK cells fail to activate and secrete IFN-gamma in response to KLR activation

• response is normal when IL-2 is used to stimulate the cells

impaired natural killer cell mediated cytotoxicity ( J:111365 )

• NK cells do not have increased cytotoxicity against target cells coated with an anti-KLR antibody

abnormal CD4-positive, alpha-beta T cell physiology ( J:112160 )

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

• these T cells also have reduced secretion of IL-2 and IFN-gamma

abnormal NK T cell physiology ( J:111365 )

• NKT cells fail to activate and secrete IFN-gamma in response to KLR activation

• response is normal when TCR stimulation is used

abnormal macrophage physiology ( J:141143 )

• bone marrow-derived macrophages fail to respond to Clec4e (Mincle) stimulation

impaired macrophage phagocytosis ( J:50023 )

• macrophages have lost the ability to ingest target cells coated in IgG

abnormal cytokine level ( J:258645 )

abnormal antigen presentation ( J:112160 )

• CD4⁺ T cells have normal primary responses suggesting lower T cell activity from immunized mice is a failure in antigen presentation

abnormal chemokine secretion ( J:141143 )

• bone marrow-derived macrophages fail to secrete MIP-2 to Clec4e (Mincle) stimulation

decreased interferon-gamma secretion ( J:111365 , J:112160 )

• natural killer and natural killer T cells fail to secrete IFN-gamma in response to KLR stimulation (J:111365)

• CD4⁺ T cells isolated from antigen-challenged mice have reduced secretion of IFN-gamma in response to antigen encounter in vitro (J:112160)

decreased interleukin-2 secretion ( J:112160 )

• CD4⁺ T cells isolated from antigen-challenged mice have reduced secretion of IL-2 in response to antigen encounter in vitro

decreased inflammatory response ( J:50023 )

• macrophages have lost the ability to ingest target cells coated in IgG

decreased susceptibility to type IV hypersensitivity reaction ( J:112160 )

• footpad swelling of antigen-sensitized mice is one-third less than controls 2 weeks after antigen challenge and one-half less than controls after 10 weeks

hematopoietic system

decreased T cell proliferation ( J:112160 )

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

decreased IgG level ( J:112160 )

decreased IgG1 level ( J:112160 )

• mice have lower titers of antigen-specific IgG1 2 weeks after immunization compared to controls

decreased IgG2a level ( J:112160 )

• mice have lower titers of antigen-specific IgG2a 2 weeks after immunization compared to controls

decreased IgG2b level ( J:112160 )

• mice have lower titers of antigen-specific IgG2b 2 weeks after immunization compared to controls

decreased IgG3 level ( J:112160 )

• mice have lower titers of antigen-specific IgG3 2 weeks after immunization compared to controls

abnormal NK cell physiology ( J:111365 )

• NK cells fail to activate and secrete IFN-gamma in response to KLR activation

• response is normal when IL-2 is used to stimulate the cells

impaired natural killer cell mediated cytotoxicity ( J:111365 )

• NK cells do not have increased cytotoxicity against target cells coated with an anti-KLR antibody

abnormal CD4-positive, alpha-beta T cell physiology ( J:112160 )

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

• these T cells also have reduced secretion of IL-2 and IFN-gamma

abnormal NK T cell physiology ( J:111365 )

• NKT cells fail to activate and secrete IFN-gamma in response to KLR activation

• response is normal when TCR stimulation is used

abnormal macrophage physiology ( J:141143 )

• bone marrow-derived macrophages fail to respond to Clec4e (Mincle) stimulation

impaired macrophage phagocytosis ( J:50023 )

• macrophages have lost the ability to ingest target cells coated in IgG

Allelic Composition	Fcer1g^tm1Tks/Fcer1g^tm1Tks
Genetic Background	involves: C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fcer1g^tm1Tks mutation (1 available); any Fcer1g mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:203159 )

• in mice treated with oil-in-water emulsion of trehalose-6,60'-dimycolate (TDM)

immune system

decreased dendritic cell number ( J:203159 )

• TDM-treated mice exhibit less of an increase in draining lymph nodes dendritic cells compared with wild-type mice

abnormal chemokine secretion ( J:203159 )

• bone marrow-derived dendritic cells and macrophages stimulated with platelets coated in trehalose-6,60'-dimycolate (TDM) or zymosan exhibit reduced MIP-2 secretion compared with wild-type cells

abnormal interferon-gamma secretion ( J:203159 )

• TDM-treated bone marrow dendritic cells co-cultured with OT-II cells and OVA323-339 or OVA257-264 peptide or ovalbumin protein fail to exhibit an increase in IFN-gamma and IL17 unlike wild-type cells

abnormal interleukin-17 secretion ( J:203159 )

• TDM-treated bone marrow dendritic cells co-cultured with OT-II cells and OVA323-339 peptide fail to exhibit an increase in IFN-gamma and IL17 unlike wild-type cells

decreased tumor necrosis factor secretion ( J:203159 )

• in bone marrow-derived dendritic cells and macrophages stimulated with platelets coated in TDM or zymosan

homeostasis/metabolism

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:203159 )

• in mice treated with oil-in-water emulsion of trehalose-6,60'-dimycolate (TDM)

decreased physiological sensitivity to xenobiotic ( J:203159 )

• mice treated with TDM exhibit are resistance to lung inflammation, granuloma and lethality unlike wild-type mice

hematopoietic system

decreased dendritic cell number ( J:203159 )

• TDM-treated mice exhibit less of an increase in draining lymph nodes dendritic cells compared with wild-type mice

Allelic Composition	Fas^lpr/Fas^lpr Fcer1g^tm1Tks/Fcer1g^tm1Tks
Genetic Background	MRL.Cg-Fcer1g^tm1Tks Fas^lpr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fas^lpr mutation (39 available); any Fas mutation (83 available)
Fcer1g^tm1Tks mutation (1 available); any Fcer1g mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:106188 )

• all mice diet of renal failure by 65 weeks of age with a 50% survival rate at a median age of 32-34 weeks similar to MRL-Fas^lpr mice

immune system

immune system phenotype ( J:106188 )

N	• MRL-Fas mice homozygous for the Fcer1g^tm1Tks allele still develop glomerulonephritis in a similar manner as MRL-Fas^lpr mice carrying the wild-type Fcer1g^tm1Tks allele

arteritis ( J:106188 )

• necrotizing vasculitis with mononuclear cell infiltration, vessel wall destruction, and occasional thrombosis are observed in the interlobular arteries of the kidney

• necrotizing vasculitis of the pulmonary arteries, with mononuclear cell infiltration and vessel wall destruction occur

increased spleen weight ( J:106188 )

• spleen weight is 7- to 8-fold greater than C57BL/6 controls but is similar to MRL-Fas^lpr mice

increased double-negative T cell number ( J:106188 )

• a double-negative, B220⁺ T cell population accumulates in the spleen and lymph nodes similar to MRL-Fas^lpr mice

increased IgG level ( J:106188 )

• IgG levels are elevated compared to C57BL/6 controls but are similar to MRL-Fas^lpr mice

decreased susceptibility to type III hypersensitivity reaction ( J:106188 )

• extravasation does not occur in mice as occurs in controls when iv injected with OVA and intradermally injected with rabbit anti-OVA IgG

increased anti-double stranded DNA antibody level ( J:106188 )

• anti-DNA Iglevels are elevated compared to C57BL/6 controls but are similar to MRL-Fas^lpr mice

glomerulonephritis ( J:106188 )

• mice develop diffuse proliferative GN with mononuclear cell infiltration, mesangial and endothelial cell proliferation, and crescent formation after 16 weeks of age similar to MRL-Fas^lpr mice

• proteinuria, followed by renal failure, develops in all mice

renal/urinary system

abnormal glomerular capillary endothelium morphology ( J:106188 )

• endothelial cell proliferation is noted after 16 weeks of age

increased mesangial cell number ( J:106188 )

• mesangial cell proliferation is noted after 16 weeks of age

increased kidney cell proliferation ( J:106188 )

• mesangial and endothelial cell proliferation after 16 weeks of age

increased urine protein level ( J:106188 )

• urinary protein concentrations increase with age similar to MRL-Fas^lpr mice

glomerulonephritis ( J:106188 )

• mice develop diffuse proliferative GN with mononuclear cell infiltration, mesangial and endothelial cell proliferation, and crescent formation after 16 weeks of age similar to MRL-Fas^lpr mice

• proteinuria, followed by renal failure, develops in all mice

glomerular crescent ( J:106188 )

• crescent formation is noted after 16 weeks of age

kidney failure ( J:106188 )

• mice die of renal failure by 65 weeks of age similar to MRL-Fas^lpr mice

homeostasis/metabolism

increased urine protein level ( J:106188 )

• urinary protein concentrations increase with age similar to MRL-Fas^lpr mice

cardiovascular system

abnormal glomerular capillary endothelium morphology ( J:106188 )

• endothelial cell proliferation is noted after 16 weeks of age

vascular inflammation ( J:106188 )

• various forms of medium and small vessel vasculitis occur similar to MRL-Fas^lpr mice

arteritis ( J:106188 )

• necrotizing vasculitis with mononuclear cell infiltration, vessel wall destruction, and occasional thrombosis are observed in the interlobular arteries of the kidney

• necrotizing vasculitis of the pulmonary arteries, with mononuclear cell infiltration and vessel wall destruction occur

hematopoietic system

increased spleen weight ( J:106188 )

• spleen weight is 7- to 8-fold greater than C57BL/6 controls but is similar to MRL-Fas^lpr mice

increased double-negative T cell number ( J:106188 )

• a double-negative, B220⁺ T cell population accumulates in the spleen and lymph nodes similar to MRL-Fas^lpr mice

increased IgG level ( J:106188 )

• IgG levels are elevated compared to C57BL/6 controls but are similar to MRL-Fas^lpr mice

cellular

increased mesangial cell number ( J:106188 )

• mesangial cell proliferation is noted after 16 weeks of age

increased kidney cell proliferation ( J:106188 )

• mesangial and endothelial cell proliferation after 16 weeks of age

growth/size/body

increased spleen weight ( J:106188 )

• spleen weight is 7- to 8-fold greater than C57BL/6 controls but is similar to MRL-Fas^lpr mice

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