Overview

Also Known As:Fasl gld

Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2019-05-22 00:00:00)

Fasl^gld

Allele Type	Gene Symbol	Gene Name
Spontaneous	Fasl	Fas ligand (TNF superfamily, member 6)

View Genetics

Research Applications

Hematological Research
Apoptosis Research
Cancer Research
Mouse/Human Gene Homologs
Cell Biology Research
Immunology, Inflammation and Autoimmunity Research

View All Research Applications

Base Price

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$128.38 Domestic price for male 4-week

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Details

Detailed Description

Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

The Cryaa^lop18 mutation was identified in the C57BL/6JSmn inbred strain in approximately 1991. This is at least 5 years from the date of the final (N10) backcross generation of B6Smn.C3-Fasl^gld/J. In 2003, four B6Smn.C3-Fasl^gld/J mice were assessed and the recessive lop18 phenotype was absent from all of them. This does not guarantee that the Cryaa^lop18 mutation is absent from this strain.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Chang E; Galle L; Maggs D; Estes DM; Mitchell WJ. 2000. Pathogenesis of herpes simplex virus type 1-induced corneal inflammation in perforin-deficient mice J Virol 74(24):11832-40PubMed: 11090183 MGI: J:65895
Davidson WF; Giese T; Fredrickson TN. 1998. Spontaneous development of plasmacytoid tumors in mice with defective Fas-Fas ligand interactions. J Exp Med 187(11):1825-38PubMed: 9607923 MGI: J:49221
Giese T; Davidson WF. 1994. Chronic treatment of C3H-lpr/lpr and C3H-gld/gld mice with anti-CD8 monoclonal antibody prevents the accumulation of double negative T cells but not autoantibody production. J Immunol 152(4):2000-10PubMed: 8120404 MGI: J:17479
Medana I; Li Z; Flugel A; Tschopp J; Wekerle H; Neumann H. 2001. Fas ligand (CD95L) protects neurons against perforin-mediated T lymphocyte cytotoxicity. J Immunol 167(2):674-81PubMed: 11441070 MGI: J:109872
Riera L; Gariglio M; Pagano M; Gaiola O; Simon MM; Landolfo S. 2001. Control of murine cytomegalovirus replication in salivary glands during acute infection is independent of the Fas ligand/Fas system. New Microbiol 24(3):231-8PubMed: 11497079 MGI: J:109866
Roths JB; Murphy ED; Eicher EM. 1984. A new mutation, gld, that produces lymphoproliferation and autoimmunity in C3H/HeJ mice. J Exp Med 159(1):1-20PubMed: 6693832 MGI: J:7306
Screpanti V; Wallin RP; Ljunggren HG; Grandien A. 2001. A central role for death receptor-mediated apoptosis in the rejection of tumors by NK cells. J Immunol 167(4):2068-73PubMed: 11489989 MGI: J:109869
Takahashi T; Tanaka M; Brannan CI; Jenkins NA; Copeland NG; Suda T; Nagata S. 1994. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76(6):969-76PubMed: 7511063 MGI: J:17445
van den Brink MR; Moore E; Horndasch KJ; Crawford JM; Murphy GF; Burakoff SJ. 2000. Fas ligand-deficient gld mice are more susceptible to graft-versus-host-disease. Transplantation 70(1):184-91PubMed: 10919598 MGI: J:63433
Wigginton JM; Lee JK; Wiltrout TA; Alvord WG; Hixon JA; Subleski J; Back TC; Wiltrout RH. 2002. Synergistic engagement of an ineffective endogenous anti-tumor immune response and induction of IFN-gamma and Fas-ligand-dependent tumor eradication by combined administration of IL-18 and IL-2. J Immunol 169(8):4467-74PubMed: 12370382 MGI: J:109850

View All References

Genetics

Fasl^gld

Allele Symbol: Fasl^gld

Allele Name	generalized lymphoproliferative disease
Allele Type	Spontaneous
Allele Synonym(s)	CD95-; FasL-; gld; Tnfsf6^gld
Gene Symbol and Name	Fasl, Fas ligand (TNF superfamily, member 6)
Gene Synonym(s)
Strain of Origin	C3H/HeJ
Chromosome	1
Molecular Note	A T-to-C transition point mutation near the 3' end of the coding sequence causes a replacement of a highly conserved phenylalanine with a leucine at position 273 (p.F273L) in the extracellular region of the encoded protein.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

autoimmune lymphoproliferative syndrome

Research Areas By Phenotype

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

Genotype: Fasl^gld related

Hematological Research
Apoptosis Research
- Extracellular Modulators
Cancer Research
- Genes Regulating Growth and Proliferation
Mouse/Human Gene Homologs
- systemic lupus erythematosus
Cell Biology Research
- Signal Transduction
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
  - lupus erythematosus

Mammalian Phenotype Terms by Genotype

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

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl/J

growth/size/body region phenotype

enlarged spleen
- evident after 13 weeks of age
- 4-fold enlargement compared to controls

hematopoietic system phenotype

abnormal T cell differentiation
- abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
- are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
- cells stimulated with Con A failed to produce IL-2
- exhibit rearrangements of beta-chain genes
- express TCR beta and alpha gene mRNA
- did not proliferate or generate CTL in response to stimulation with alloantigens
- bind at high levels lectins that normally bind preferentially to B cells
- express beta-chain of TCR

anemia
- evident in 40% of animals autopsied when moribund

increased IgG1 level

increased IgM level

increased IgG level
- 10-fold IgG2a
- 3- to 6-fold IgG1 and IgG2b

increased immunoglobulin level
- developed broad-based hypergammaglobulinemia
- development of broad-based hypergammaglobulinemia

increased lymphocyte cell number
- 4-fold greater than controls
- 5-fold increase in peripheral blood lymphocytes

decreased cytotoxic T cell cytolysis
- in Fas-dependent lysis assays, but not allogeneic targets

increased IgA level
- 10-fold

increased IgG2b level

increased T cell number
- 59 to 68%

enlarged spleen
- evident after 13 weeks of age
- 4-fold enlargement compared to controls

increased neutrophil cell number
- 2-fold greater than controls

decreased B cell number
- 36 to 15%

increased IgG2a level

increased leukocyte cell number

homeostasis/metabolism phenotype

skin edema
- ~25% of those autopsied when moribund showed marked subcutaneous edema

immune system phenotype

abnormal lymph node morphology

increased anti-nuclear antigen antibody level
- high titers of antinuclear autoantibodies evident at 14 weeks of age
- high titers of antinuclear autoantibodies evident by 16 weeks of age in all mice assayed

abnormal T cell differentiation
- express beta-chain of TCR
- cells stimulated with Con A failed to produce IL-2
- abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
- are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
- bind at high levels lectins that normally bind preferentially to B cells
- did not proliferate or generate CTL in response to stimulation with alloantigens
- express TCR beta and alpha gene mRNA
- exhibit rearrangements of beta-chain genes

decreased B cell number
- 36 to 15%

increased IgG1 level

increased IgG2b level

increased IgM level

increased T cell number
- 59 to 68%

enlarged lymph nodes
- enlarged peripheral lymph nodes evident at 13 weeks of age, abdominal evident shortly thereafter
- evidence of chronic inflammation at autopsy, with proliferation of lymphocytes and admixtures of histiocytes and plasma cells observed, fibrosis and multinucleated giant cells also frequently observed
- 50-fold heavier at 20 weeks of age than controls

enlarged spleen
- evident after 13 weeks of age
- 4-fold enlargement compared to controls

increased anti-double stranded DNA antibody level
- high concentrations of anti-dsDNA autoantibodies present

increased neutrophil cell number
- 2-fold greater than controls

increased IgA level
- 10-fold

increased IgG level
- 10-fold IgG2a
- 3- to 6-fold IgG1 and IgG2b

increased immunoglobulin level
- development of broad-based hypergammaglobulinemia
- developed broad-based hypergammaglobulinemia

decreased cytotoxic T cell cytolysis
- in Fas-dependent lysis assays, but not allogeneic targets

increased leukocyte cell number

increased autoantibody level
- thymocyte-binding autoantibody present

increased lymphocyte cell number
- 4-fold greater than controls
- 5-fold increase in peripheral blood lymphocytes

interstitial pneumonia
- lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund

increased IgG2a level

integument phenotype

skin edema
- ~25% of those autopsied when moribund showed marked subcutaneous edema

mammalian phenotype

renal/urinary system phenotype
- Normal - despite glomerular deposition of immune complexes, no, or very little, glomerulonephritis was observed

neoplasm
- Normal - regression of transplanted SCCVII tumors by gene therapy treatment with Il12b is normal

cardiovascular system phenotype
- Normal - no defect detected: no vascular disease, including necrotizing arteritis or polyarteritis

mortality/aging
- Normal - when placed under hyperoxic conditions for >5 days, mice do not show increased survival (resistance to hyperoxia) compared to wild-type mice

mortality/aging

premature death
- males survived to mean age of 396 days, females to 369 days, controls survived until 688 days

respiratory system phenotype

interstitial pneumonia
- lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl

immune system phenotype

abnormal T cell physiology
- cells do not generate CTL in response to stimulation with alloantigens

abnormal T cell morphology
- lymph node cells (T cell origin) are abnormal; cells are Ly-2^-/L3T4^-/surface Ig^-

abnormal interleukin level
- stimulation with concanavalin A does not induce cells to produce Il2

abnormal T cell proliferation
- cells do not proliferate in response to stimulation with alloantigens

nervous system phenotype

decreased neuron apoptosis
- neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death
- very low levels of apoptosis (15%) compared to wild-type (60%) are seen when cortical neurons are treated with Abeta25-35 or Abeta1-40 peptides

cellular phenotype

decreased neuron apoptosis
- neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death
- very low levels of apoptosis (15%) compared to wild-type (60%) are seen when cortical neurons are treated with Abeta25-35 or Abeta1-40 peptides

abnormal T cell proliferation
- cells do not proliferate in response to stimulation with alloantigens

hematopoietic system phenotype

abnormal T cell morphology
- lymph node cells (T cell origin) are abnormal; cells are Ly-2^-/L3T4^-/surface Ig^-

abnormal T cell physiology
- cells do not generate CTL in response to stimulation with alloantigens

abnormal T cell proliferation
- cells do not proliferate in response to stimulation with alloantigens

homeostasis/metabolism phenotype

abnormal interleukin level
- stimulation with concanavalin A does not induce cells to produce Il2

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * C57BL/6

growth/size/body region phenotype

enlarged spleen
- by 14 weeks

homeostasis/metabolism phenotype

decreased susceptibility to injury
- following pancreatic duct ligation, mice exhibit virtually no acinar cell loss or ductal metaplasia compared with similarly treated wild-type mice
- following pancreatic duct ligation, mice exhibit less acinar cell apoptosis than similarly treated wild-type mice
- Normal - however, areas of inflammation and fibrosis are sometimes observed following pancreatic duct ligation

increased circulating tumor necrosis factor level

immune system phenotype

increased circulating tumor necrosis factor level

dermatitis
- in 10% of mice and later than in Fasl^tm1.1Ast homozygotes

enlarged spleen
- by 14 weeks

increased IgG1 level

increased IgG2b level

increased IgG2a level

increased T cell number
- TCRalpha/beta+CD4-CD8-B220+ T cells

increased anti-nuclear antigen antibody level
- in some mice

increased IgE level

increased susceptibility to systemic lupus erythematosus
- by 57 weeks, 15% of mice develop fatal SLE-like autoimmune kidney disease unlike wild-type mice

enlarged lymph nodes
- by 14 weeks

increased IgG level

integument phenotype

dermatitis
- in 10% of mice and later than in Fasl^tm1.1Ast homozygotes

mammalian phenotype

immune system phenotype
- Normal - mice mount a normal immune response to influenza

mortality/aging

premature death

neoplasm

increased histiocytic sarcoma incidence
- rare

hematopoietic system phenotype

increased T cell number
- TCRalpha/beta+CD4-CD8-B220+ T cells

increased IgG2a level

increased IgG2b level

enlarged spleen
- by 14 weeks

increased IgG1 level

increased IgE level

increased IgG level

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ

skeleton phenotype

abnormal osteoclast physiology
- 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture

growth/size/body region phenotype

increased spleen weight

enlarged spleen

hematopoietic system phenotype

increased spleen weight

enlarged spleen

abnormal osteoclast physiology
- 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture

immune system phenotype

enlarged spleen

enlarged lymph nodes

increased spleen weight

abnormal osteoclast physiology
- 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * CBA

mammalian phenotype

reproductive system phenotype
- Normal - ediated vaginal cell death
- Normal - at 2 days after estrogen deprivation induced by gonadectomy, mutant females show a normal estrous cycle and a similar degree of vaginal regression (as measured by the decrease in vaginal organ weight) relative to wild-type females, indicating normal Fas-mediated vaginal cell death

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

Genotype: Fasl^gld/Fasl^gld
B6Smn.C3-Fasl/J

cellular phenotype

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

focal hepatic necrosis
- necroinflammatory foci after BDL are reduced in number compared to controls after BDL

immune system phenotype

increased susceptibility to viral infection
- inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days

abnormal NK cell physiology
- continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver

brain inflammation
- by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)
- at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
- tissue damage is less frequent at 45 days than in Prf-null mice

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

increased susceptibility to bacterial infection
- mice infected with 500 CFU of S. aureus have drastically elevated number of S. aureus CFU compared to similarly-infected wild-type mice

increased susceptibility to Picornaviridae infection
- inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days

CNS inflammation
- by 7 days after TMEV infection, inflammation is present in the meninges and gray matter, but decreases by 21 days, although not as much as in controls (B6)

decreased granulocyte number
- mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

eye inflammation
- mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction
- mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection

liver/biliary system phenotype

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

focal hepatic necrosis
- necroinflammatory foci after BDL are reduced in number compared to controls after BDL

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

abnormal hepatocyte morphology
- confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL

nervous system phenotype

brain inflammation
- by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)
- at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
- tissue damage is less frequent at 45 days than in Prf-null mice

demyelination
- at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice

CNS inflammation
- by 7 days after TMEV infection, inflammation is present in the meninges and gray matter, but decreases by 21 days, although not as much as in controls (B6)

reproductive system phenotype

abnormal sperm number
- epididymal sperm count is increased compared to in wild-type mice due to decreased sperm apoptosis

abnormal sperm physiology
- sperm apoptosis is decreased compared to in wild-type mice

hematopoietic system phenotype

abnormal NK cell physiology
- continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver

decreased granulocyte number
- mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

skeleton phenotype

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

vision/eye phenotype

abnormal eye electrophysiology
- mice have only 7% of b-wave amplitude remaining at 24 hours after infection with 500CFU S. aureus, and show no detectable retinal function after this time point

eye inflammation
- mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
- mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction

homeostasis/metabolism phenotype

decreased circulating alanine transaminase level
- one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls

Genotype: Fasl^gld/Fasl^gld
B6.C3-Fasl

immune system phenotype

impaired macrophage phagocytosis
- mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice
- clearance of apoptotic material by macrophages is reduced

increased spleen weight

abnormal lymph node morphology
- mutants exhibit an increase in apoptotic material in the lymph nodes

enlarged lymph nodes
- increase in lymph node size and weight

enlarged spleen

increased anti-nuclear antigen antibody level
- high titers of anti-nuclear antigen antibodies (ANAs) on normal and Western diet

increased autoantibody level
- serum levels of anticardiolipin antibody are modestly elevated on a normal diet and are further elevated on a Western diet

mammalian phenotype

cardiovascular system phenotype
- Normal - mutants do not develop atherosclerotic lesions and do not show macrophage or T cell infiltration in the aorta

homeostasis/metabolism phenotype
- Normal - lipid levels are normal

cellular phenotype

impaired macrophage phagocytosis
- mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice
- clearance of apoptotic material by macrophages is reduced

increased apoptosis
- mutants exhibit an increase in apoptotic material in the lymph nodes

growth/size/body region phenotype

enlarged spleen

increased spleen weight

hematopoietic system phenotype

impaired macrophage phagocytosis
- mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice
- clearance of apoptotic material by macrophages is reduced

increased spleen weight

enlarged spleen

References

Chang E; Galle L; Maggs D; Estes DM; Mitchell WJ. 2000. Pathogenesis of herpes simplex virus type 1-induced corneal inflammation in perforin-deficient mice J Virol 74(24):11832-40PubMed: 11090183 MGI: J:65895
Davidson WF; Giese T; Fredrickson TN. 1998. Spontaneous development of plasmacytoid tumors in mice with defective Fas-Fas ligand interactions. J Exp Med 187(11):1825-38PubMed: 9607923 MGI: J:49221
Giese T; Davidson WF. 1994. Chronic treatment of C3H-lpr/lpr and C3H-gld/gld mice with anti-CD8 monoclonal antibody prevents the accumulation of double negative T cells but not autoantibody production. J Immunol 152(4):2000-10PubMed: 8120404 MGI: J:17479
Medana I; Li Z; Flugel A; Tschopp J; Wekerle H; Neumann H. 2001. Fas ligand (CD95L) protects neurons against perforin-mediated T lymphocyte cytotoxicity. J Immunol 167(2):674-81PubMed: 11441070 MGI: J:109872
Riera L; Gariglio M; Pagano M; Gaiola O; Simon MM; Landolfo S. 2001. Control of murine cytomegalovirus replication in salivary glands during acute infection is independent of the Fas ligand/Fas system. New Microbiol 24(3):231-8PubMed: 11497079 MGI: J:109866
Roths JB; Murphy ED; Eicher EM. 1984. A new mutation, gld, that produces lymphoproliferation and autoimmunity in C3H/HeJ mice. J Exp Med 159(1):1-20PubMed: 6693832 MGI: J:7306
Screpanti V; Wallin RP; Ljunggren HG; Grandien A. 2001. A central role for death receptor-mediated apoptosis in the rejection of tumors by NK cells. J Immunol 167(4):2068-73PubMed: 11489989 MGI: J:109869
Takahashi T; Tanaka M; Brannan CI; Jenkins NA; Copeland NG; Suda T; Nagata S. 1994. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76(6):969-76PubMed: 7511063 MGI: J:17445
van den Brink MR; Moore E; Horndasch KJ; Crawford JM; Murphy GF; Burakoff SJ. 2000. Fas ligand-deficient gld mice are more susceptible to graft-versus-host-disease. Transplantation 70(1):184-91PubMed: 10919598 MGI: J:63433
Wigginton JM; Lee JK; Wiltrout TA; Alvord WG; Hixon JA; Subleski J; Back TC; Wiltrout RH. 2002. Synergistic engagement of an ineffective endogenous anti-tumor immune response and induction of IFN-gamma and Fas-ligand-dependent tumor eradication by combined administration of IL-18 and IL-2. J Immunol 169(8):4467-74PubMed: 12370382 MGI: J:109850

Additional References

Alexander CE; Kaye PM; Engwerda CR. 2001. CD95 is required for the early control of parasite burden in the liver of Leishmania donovani-infected mice. Eur J Immunol 31(4):1199-210PubMed: 11298345 MGI: J:68808
Dalton JE; Howell G; Pearson J; Scott P; Carding SR. 2004. Fas-Fas ligand interactions are essential for the binding to and killing of activated macrophages by gammadelta T cells. J Immunol 173(6):3660-7PubMed: 15356111 MGI: J:92754
Gorbachev AV; Fairchild RL. 2004. CD4(+) T cells regulate CD8(+) T cell-mediated cutaneous immune responses by restricting effector T cell development through a Fas ligand-dependent mechanism. J Immunol 172(4):2286-95PubMed: 14764697 MGI: J:88048
Hawes NL; Chang B; Hageman GS; Nusinowitz S; Nishina PM; Schneider BS; Smith RS; Roderick TH; Davisson MT; Heckenlively JR. 2000. Retinal degeneration 6 (rd6): a new mouse model for human retinitis punctata albescens. Invest Ophthalmol Vis Sci 41(10):3149-57PubMed: 10967077 MGI: J:64087
Hori J; Joyce NC; Streilein JW. 2000. Immune privilege and immunogenicity reside among different layers of the mouse cornea. Invest Ophthalmol Vis Sci 41(10):3032-42PubMed: 10967061 MGI: J:64197
Ma Y; Liu H; Tu-Rapp H; Thiesen HJ; Ibrahim SM; Cole SM; Pope RM. 2004. Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation. Nat Immunol 5(4):380-7PubMed: 15004557 MGI: J:89208
Takeda K; Hayakawa Y; Van Kaer L; Matsuda H; Yagita H; Okumura K. 2000. Critical contribution of liver natural killer T cells to a murine model of hepatitis. Proc Natl Acad Sci U S A 97(10):5498-503PubMed: 10792025 MGI: J:62215

Additional - Fasl^gld related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Restriction Enzyme Digest:Fasl
- End Point Analysis:Fasl
- Genotyping resources and troubleshooting
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 Fasl gld mouse strain in a publication, please cite the originating article(s) and include JAX stock #001021 in your Materials and Methods section.

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AX4 (Standard)

AX18 (Maximum)

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weeks

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Also Known As:Fasl gld

Genetic overview

Research Applications

Base Price

Detailed Description

Control Suggestions

Additional Information

Selected References

Faslgld

Allele Symbol: Faslgld

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

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

Genotype: Faslgld related

Mammalian Phenotype Terms by Genotype

Genotype: Faslgld/FaslgldC3H/HeJ-Fasl/J

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

integument phenotype

mammalian phenotype

mortality/aging

respiratory system phenotype

Genotype: Faslgld/FaslgldC3H/HeJ-Fasl

immune system phenotype

nervous system phenotype

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ * C57BL/6

growth/size/body region phenotype

homeostasis/metabolism phenotype

immune system phenotype

integument phenotype

mammalian phenotype

mortality/aging

neoplasm

hematopoietic system phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ

skeleton phenotype

growth/size/body region phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ * CBA

mammalian phenotype

Genotype: Faslgld/FaslgldB6Smn.C3-Fasl/J

cellular phenotype

immune system phenotype

liver/biliary system phenotype

nervous system phenotype

reproductive system phenotype

hematopoietic system phenotype

skeleton phenotype

vision/eye phenotype

homeostasis/metabolism phenotype

Genotype: Faslgld/FaslgldB6.C3-Fasl

immune system phenotype

mammalian phenotype

cellular phenotype

growth/size/body region phenotype

hematopoietic system phenotype

References

Additional References

Additional - Faslgld related

Genotyping Protocols

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Fasl^gld

Allele Symbol: Fasl^gld

Genotype: Fasl^gld related

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl/J

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * C57BL/6

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * CBA

Genotype: Fasl^gld/Fasl^gld
B6Smn.C3-Fasl/J

Genotype: Fasl^gld/Fasl^gld
B6.C3-Fasl

Additional - Fasl^gld related