JAX Mouse Strain Datasheet - 000784

C3H/HeJ-Fasl^gld/J

Stock No:: 000784

Cryo Recovery

Overview

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.

Genetic overview

Genetic Background	Generation

Fasl^gld

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

View Genetics

Research Applications

Apoptosis Research
Cancer Research
Cell Biology Research
Hematological Research
Immunology, Inflammation and Autoimmunity Research

View All Research Applications

Base Price

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Details

Important Note

This strain is homozygous for the retinal degeneration allele Pde6b^rd1.

Detailed Description

Control Suggestions

000659 C3H/HeJ

Additional Information

Considerations for Choosing Controls

Selected References

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):1825-38. PubMed: 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):2000-10. PubMed: 8120404 MGI: J:17479
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):1-20. PubMed: 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):2068-73. PubMed: 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):969-76. PubMed: 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):184-91. PubMed: 10919598 MGI: J:63433

View All References

Genetics

Fasl^gld

Allele Symbol: Fasl^gld

Allele Name	generalized lymphoproliferative disease
Allele Type	Spontaneous
Allele Synonym(s)	CD95-; FasL-; Tnfsf6^gld; gld
Gene Symbol and Name	Fasl, Fas ligand (TNF superfamily, member 6)
Gene Synonym(s)	ALPS1B; APT1LG1; APTL; Apt1Lg1; CD178; CD95-L; CD95L; FASL; Fas antigen ligand; Fas-L; TNFSF6; TNLG1A; Tnfsf6; Tnfsf6; Tnlg1a; generalized lymphoproliferative disease; gld; tumor necrosis factor (ligand) superfamily, member 6
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 in the extracellular region of the encoded protein.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Fasl^gld related

Apoptosis Research
- Extracellular Modulators
Cancer Research
- Genes Regulating Growth and Proliferation
Cell Biology Research
- Signal Transduction
Hematological Research
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
  - lupus erythematosus

Mammalian Phenotype Terms by Genotype

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

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

immune 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

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

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

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

immune system phenotype

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

enlarged lymph nodes

enlarged spleen

increased spleen weight

skeleton phenotype

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

hematopoietic system phenotype

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

enlarged spleen

increased spleen weight

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

mortality/aging

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

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

cardiovascular system phenotype

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

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+
- bind at high levels lectins that normally bind preferentially to B cells
- cells stimulated with Con A failed to produce IL-2
- did not proliferate or generate CTL in response to stimulation with alloantigens
- exhibit rearrangements of beta-chain genes
- express TCR beta and alpha gene mRNA
- express beta-chain of TCR

anemia
- evident in 40% of animals autopsied when moribund

decreased B cell number
- 36 to 15%

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

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

increased IgA level
- 10-fold

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

increased IgG1 level

increased IgG2a level

increased IgG2b level

increased IgM level

increased T cell number
- 59 to 68%

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

increased leukocyte cell number

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

increased neutrophil cell number
- 2-fold greater than controls

homeostasis/metabolism phenotype

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

immune 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+
- bind at high levels lectins that normally bind preferentially to B cells
- cells stimulated with Con A failed to produce IL-2
- did not proliferate or generate CTL in response to stimulation with alloantigens
- exhibit rearrangements of beta-chain genes
- express TCR beta and alpha gene mRNA
- express beta-chain of TCR

abnormal lymph node morphology

decreased B cell number
- 36 to 15%

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

enlarged lymph nodes
- 50-fold heavier at 20 weeks of age than controls
- 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

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

increased IgA level
- 10-fold

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

increased IgG1 level

increased IgG2a level

increased IgG2b level

increased IgM level

increased T cell number
- 59 to 68%

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

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

increased autoantibody level
- thymocyte-binding autoantibody present

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

increased leukocyte cell number

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

increased neutrophil cell number
- 2-fold greater than controls

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

renal/urinary system phenotype

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

respiratory system phenotype

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

neoplasm

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

integument phenotype

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

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

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

immune system phenotype

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)

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

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

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

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

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

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

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

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

liver/biliary system phenotype

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

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

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

nervous system phenotype

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)

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

homeostasis/metabolism phenotype

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

hematopoietic system phenotype

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

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

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

skeleton phenotype

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

cellular phenotype

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

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

immune system phenotype

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

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

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

increased spleen weight

cellular phenotype

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

hematopoietic system phenotype

enlarged spleen

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

increased spleen weight

homeostasis/metabolism phenotype

homeostasis/metabolism phenotype
- lipid levels are normal

cardiovascular system phenotype

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

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

mortality/aging

premature death

immune system phenotype

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

enlarged lymph nodes
- by 14 weeks

enlarged spleen
- by 14 weeks

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

increased IgE level

increased IgG level

increased IgG1 level

increased IgG2a level

increased IgG2b level

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

increased anti-nuclear antigen antibody level
- in some mice

increased circulating tumor necrosis factor level

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

neoplasm

increased histiocytic sarcoma incidence
- rare

homeostasis/metabolism phenotype

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

increased circulating tumor necrosis factor level

hematopoietic system phenotype

enlarged spleen
- by 14 weeks

increased IgE level

increased IgG level

increased IgG1 level

increased IgG2a level

increased IgG2b level

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

integument phenotype

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

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

reproductive system phenotype

reproductive system phenotype
- 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 deathediated vaginal cell death

References

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):1825-38. PubMed: 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):2000-10. PubMed: 8120404 MGI: J:17479
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):1-20. PubMed: 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):2068-73. PubMed: 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):969-76. PubMed: 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):184-91. PubMed: 10919598 MGI: J:63433

Additional - Fasl^gld related

Akiyama K; Chen C; Wang D; Xu X; Qu C; Yamaza T; Cai T; Chen W; Sun L; Shi S. 2012. Mesenchymal-stem-cell-induced immunoregulation involves FAS-ligand-/FAS-mediated T cell apoptosis. Cell Stem Cell 10(5):544-55. PubMed: 22542159 MGI: J:185809
Alard P; Clark SL; Kosiewicz MM. 2004. Mechanisms of tolerance induced by TGF beta-treated APC: CD4 regulatory T cells prevent the induction of the immune response possibly through a mechanism involving TGF beta. Eur J Immunol 34(4):1021-30. PubMed: 15048712 MGI: J:115475
Alenzi FQ; Marley SB; Lewis JL; Chandrashekran A; Warrens AN; Goldman JM; Gordon MY. 2002. A role for the Fas/Fas ligand apoptotic pathway in regulating myeloid progenitor cell kinetics. Exp Hematol 30(12):1428-35. PubMed: 12482505 MGI: J:118008
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):1199-210. PubMed: 11298345 MGI: J:68808
Allen HL; Deepe GS Jr. 2005. Apoptosis modulates protective immunity to the pathogenic fungus Histoplasma capsulatum. J Clin Invest 115(10):2875-85. PubMed: 16151533 MGI: J:101533
Alsharifi M; Lobigs M; Simon MM; Kersten A; Muller K; Koskinen A; Lee E; Mullbacher A. 2006. NK cell-mediated immunopathology during an acute viral infection of the CNS. Eur J Immunol 36(4):887-96. PubMed: 16541469 MGI: J:114787
Aprahamian T; Bonegio R; Rizzo J; Perlman H; Lefer DJ; Rifkin IR; Walsh K. 2006. Simvastatin treatment ameliorates autoimmune disease associated with accelerated atherosclerosis in a murine lupus model. J Immunol 177(5):3028-34. PubMed: 16920939 MGI: J:139547
Aprahamian T; Rifkin I; Bonegio R; Hugel B; Freyssinet JM; Sato K; Castellot JJ Jr; Walsh K. 2004. Impaired Clearance of Apoptotic Cells Promotes Synergy between Atherogenesis and Autoimmune Disease. J Exp Med 199(8):1121-31. PubMed: 15096538 MGI: J:91058
Apte RS; Richter J; Herndon J; Ferguson TA. 2006. Macrophages inhibit neovascularization in a murine model of age-related macular degeneration. PLoS Med 3(8):e310. PubMed: 16903779 MGI: J:134144
Bachmann R; Eugster HP; Frei K; Fontana A; Lassmann H. 1999. Impairment of TNF-receptor-1 signaling but not fas signaling diminishes T-cell apoptosis in myelin oligodendrocyte glycoprotein peptide-induced chronic demyelinating autoimmune encephalomyelitis in mice. Am J Pathol 154(5):1417-22. PubMed: 10329594 MGI: J:114241
Baker MB; Altman NH; Podack ER; Levy RB. 1996. The role of cell-mediated cytotoxicity in acute GVHD after MHC-matched allogeneic bone marrow transplantation in mice. J Exp Med 183(6):2645-56. PubMed: 8676085 MGI: J:33612
Balkow S; Kersten A; Tran TT; Stehle T; Grosse P; Museteanu C; Utermohlen O; Pircher H; von Weizsacker F; Wallich R; Mullbacher A; Simon MM. 2001. Concerted action of the FasL/Fas and perforin/granzyme A and B pathways is mandatory for the development of early viral hepatitis but not for recovery from viral infection. J Virol 75(18):8781-91. PubMed: 11507223 MGI: J:71217
Bangale Y; Karle S; Planque S; Zhou YX; Taguchi H; Nishiyama Y; Li L; Kalaga R; Paul S. 2003. VIPase autoantibodies in Fas-defective mice and patients with autoimmune disease. FASEB J 17(6):628-35. PubMed: 12665475 MGI: J:82662
Barreiro R; Luker G; Herndon J; Ferguson TA. 2004. Termination of antigen-specific immunity by CD95 ligand (Fas ligand) and IL-10. J Immunol 173(3):1519-25. PubMed: 15265879 MGI: J:92022
Beamer CA; Holian A. 2007. Antigen-presenting cell population dynamics during murine silicosis. Am J Respir Cell Mol Biol 37(6):729-38. PubMed: 17641296 MGI: J:141645
Bhandoola A; Dolnick B; Fayad N; Nussenzweig A; Singer A. 2000. Immature thymocytes undergoing receptor rearrangements are resistant to an Atm-dependent death pathway activated in mature T cells by double-stranded DNA breaks. J Exp Med 192(6):891-7. PubMed: 10993919 MGI: J:112013
Bhandoola A; Yui K; Siegel RM; Zerva L; Greene MI. 1994. Gld and lpr mice: single gene mutant models for failed self tolerance. Int Rev Immunol 11(3):231-44. PubMed: 7930847 MGI: J:21989
Bitsaktsis C; Winslow G. 2006. Fatal recall responses mediated by CD8 T cells during intracellular bacterial challenge infection. J Immunol 177(7):4644-51. PubMed: 16982903 MGI: J:139316
Blazar BR; Carreno BM; Panoskaltsis-Mortari A; Carter L; Iwai Y; Yagita H; Nishimura H; Taylor PA. 2003. Blockade of programmed death-1 engagement accelerates graft-versus-host disease lethality by an IFN-gamma-dependent mechanism. J Immunol 171(3):1272-7. PubMed: 12874215 MGI: J:120213
Blazar BR; Lees CJ; Martin PJ; Noelle RJ; Kwon B; Murphy W; Taylor PA. 2000. Host T cells resist graft-versus-host disease mediated by donor leukocyte infusions. J Immunol 165(9):4901-9. PubMed: 11046015 MGI: J:118027
Booker JK; Reap EA; Cohen PL. 1998. Expression and function of Fas on cells damaged by gamma-irradiation in B6 and B6/lpr mice. J Immunol 161(9):4536-41. PubMed: 9794379 MGI: J:112150
Borges VM; Falcao H; Leite-Junior JH; Alvim L; Teixeira GP; Russo M; Nobrega AF; Lopes MF; Rocco PM; Davidson WF; Linden R; Yagita H; Zin WA; DosReis GA. 2001. Fas ligand triggers pulmonary silicosis. J Exp Med 194(2):155-64. PubMed: 11457890 MGI: J:118034
Bossaller L; Rathinam VA; Bonegio R; Chiang PI; Busto P; Wespiser AR; Caffrey DR; Li QZ; Mohan C; Fitzgerald KA; Latz E; Marshak-Rothstein A. 2013. Overexpression of membrane-bound fas ligand (CD95L) exacerbates autoimmune disease and renal pathology in pristane-induced lupus. J Immunol 191(5):2104-14. PubMed: 23918976 MGI: J:205801
Bowne WB; Srinivasan R; Wolchok JD; Hawkins WG; Blachere NE; Dyall R; Lewis JJ; Houghton AN. 1999. Coupling and uncoupling of tumor immunity and autoimmunity. J Exp Med 190(11):1717-22. PubMed: 10587362 MGI: J:115120
Brochard V; Combadiere B; Prigent A; Laouar Y; Perrin A; Beray-Berthat V; Bonduelle O; Alvarez-Fischer D; Callebert J; Launay JM; Duyckaerts C; Flavell RA; Hirsch EC; Hunot S. 2009. Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease. J Clin Invest 119(1):182-92. PubMed: 19104149 MGI: J:144702
Cai Z; Yang F; Yu L; Yu Z; Jiang L; Wang Q; Yang Y; Wang L; Cao X; Wang J. 2012. Activated T cell exosomes promote tumor invasion via Fas signaling pathway. J Immunol 188(12):5954-61. PubMed: 22573809 MGI: J:188880
Camacho IA; Singh N; Hegde VL; Nagarkatti M; Nagarkatti PS. 2005. Treatment of mice with 2,3,7,8-tetrachlorodibenzo-p-dioxin leads to aryl hydrocarbon receptor-dependent nuclear translocation of NF-kappaB and expression of Fas ligand in thymic stromal cells and consequent apoptosis in T cells. J Immunol 175(1):90-103. PubMed: 15972635 MGI: J:100624
Capitini CM; Nasholm NM; Duncan BB; Guimond M; Fry TJ. 2013. Graft-versus-host disease impairs vaccine responses through decreased CD4+ and CD8+ T cell proliferation and increased perforin-mediated CD8+ T cell apoptosis. J Immunol 190(3):1351-9. PubMed: 23275602 MGI: J:193034
Chakour R; Guler R; Bugnon M; Allenbach C; Garcia I; Mauel J; Louis J; Tacchini-Cottier F. 2003. Both the Fas ligand and inducible nitric oxide synthase are needed for control of parasite replication within lesions in mice infected with Leishmania major whereas the contribution of tumor necrosis factor is minimal. Infect Immun 71(9):5287-95. PubMed: 12933876 MGI: J:85214
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Zhang HG; Fleck M; Kern ER; Liu D; Wang Y; Hsu HC; Yang P; Wang Z; Curiel DT; Zhou T; Mountz JD. 2000. Antigen presenting cells expressing Fas ligand down-modulate chronic inflammatory disease in Fas ligand-deficient mice. J Clin Invest 105(6):813-21. PubMed: 10727450 MGI: J:61112
Zhang JQ; Okumura C; McCarty T; Shin MS; Mukhopadhyay P; Hori M; Torrey TA; Naghashfar Z; Zhou JX; Lee CH; Roopenian DC; Morse HC 3rd; Davidson WF. 2004. Evidence for selective transformation of autoreactive immature plasma cells in mice deficient in Fasl. J Exp Med 200(11):1467-78. PubMed: 15583018 MGI: J:94696
Zhang Y; Xu G; Zhang L; Roberts AI; Shi Y. 2008. Th17 cells undergo fas-mediated activation-induced cell death independent of IFN-gamma. J Immunol 181(1):190-6. PubMed: 18566384 MGI: J:137178
Zhao DM; Thornton AM; DiPaolo RJ; Shevach EM. 2006. Activated CD4+CD25+ T cells selectively kill B lymphocytes. Blood 107(10):3925-32. PubMed: 16418326 MGI: J:132735
Zhou Z; Wu M; Barrett RP; McClellan SA; Zhang Y; Hazlett LD. 2010. Role of the Fas pathway in Pseudomonas aeruginosa keratitis. Invest Ophthalmol Vis Sci 51(5):2537-47. PubMed: 20019368 MGI: J:164107
Zuliani C; Kleber S; Klussmann S; Wenger T; Kenzelmann M; Schreglmann N; Martinez A; del Rio JA; Soriano E; Vodrazka P; Kuner R; Groene HJ; Herr I; Krammer PH; Martin-Villalba A. 2006. Control of neuronal branching by the death receptor CD95 (Fas/Apo-1). Cell Death Differ 13(1):31-40. PubMed: 16003386 MGI: J:121029
de Oliveira GM; Diniz RL; Batista W; Batista MM; Bani Correa C; de Araujo-Jorge TC; Henriques-Pons A. 2007. Fas ligand-dependent inflammatory regulation in acute myocarditis induced by Trypanosoma cruzi infection. Am J Pathol 171(1):79-86. PubMed: 17591955 MGI: J:122837

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Control Suggestions

Additional Information

Selected References

Faslgld

Allele Symbol: Faslgld

Disease Terms

Research Areas By Genotype

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

Genotype: Faslgld related

Mammalian Phenotype Terms by Genotype

Genotype: Faslgld/FaslgldC3H/HeJ-Faslgld

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

cellular phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ

immune system phenotype

skeleton phenotype

hematopoietic system phenotype

Genotype: Faslgld/FaslgldC3H/HeJ-Faslgld/J

mortality/aging

cardiovascular system phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

renal/urinary system phenotype

respiratory system phenotype

neoplasm

integument phenotype

Genotype: Faslgld/FaslgldB6Smn.C3-Faslgld/J

immune system phenotype

reproductive system phenotype

liver/biliary system phenotype

vision/eye phenotype

nervous system phenotype

homeostasis/metabolism phenotype

hematopoietic system phenotype

skeleton phenotype

cellular phenotype

Genotype: Faslgld/FaslgldB6.C3-Faslgld

immune system phenotype

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

cardiovascular system phenotype

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

mortality/aging

immune system phenotype

neoplasm

homeostasis/metabolism phenotype

hematopoietic system phenotype

integument phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ * CBA

reproductive system phenotype

References

Additional - Faslgld related

Genotyping Protocols

Appearance

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Fasl^gld

Allele Symbol: Fasl^gld

Genotype: Fasl^gld related

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

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

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

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

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

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

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

Additional - Fasl^gld related