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The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names C3H/HeJ-Tnfsf6gld/J    (Changed: 14-MAR-05 )
Fasgld    (Changed: 15-DEC-04 )
Type Coisogenic; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
H2 Haplotypek
Generation Definitions

Related Genotype: A/A

Important Note
This strain is homozygous for the retinal degeneration allele Pde6brd1.

Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr 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.

Control Information

   000659 C3H/HeJ
  Considerations for Choosing Controls

Related Strains

Strains carrying   Faslgld allele
001021   B6Smn.C3-Faslgld/J
002932   CPt.C3-Faslgld/J
008223   NOD.C3(B6)-Faslgld /LwnJ
View Strains carrying   Faslgld     (3 strains)

Strains carrying   Pde6brd1 allele
004202   B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J
000002   B6.C3-Pde6brd1 Hps4le/J
001022   B6C3FeF1/J a/a
000652   BDP/J
000653   BUB/BnJ
002439   C3.129P2(B6)-B2mtm1Unc/J
005494   C3.129S1(B6)-Grm1rcw/J
000509   C3.Cg-Lystbg-2J/J
000480   C3.MRL-Faslpr/J
001957   C3A Pde6brd1.O20/A-Prph2Rd2/J
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
003968   C3Bir.129P2(B6)-Il10tm1Cgn/LtJ
006435   C3Fe.SW-Soaa/MonJ
001904   C3H-Atcayji-hes/J
000659   C3H/HeJ
000511   C3H/HeJ-Ap3d1mh-2J/J
002433   C3H/HeJ-Sptbn4qv-lnd2J/J
005972   C3H/HeJBirLtJ
001824   C3H/HeJSxJ
000635   C3H/HeOuJ
000474   C3H/HeSn
001431   C3H/HeSn-ocd/J
000661   C3H/HeSnJ
002333   C3H/HeSnJ-gri/J
001576   C3He-Atp7btx-J/J
000658   C3HeB/FeJ
002588   C3HeB/FeJ-Eya1bor/J
001533   C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J
001908   C3HfB/BiJ
001502   C3Sn.B6-Epha4rb/EiGrsrJ
002235   C3Sn.C3-Ctnna2cdf/J
001547   C3Sn.Cg-Cm/J
001906   C3fBAnl.Cg-Catb/AnlJ
000656   CBA/J
000813   CBA/J-Atp7aMo-pew/J
000660   DA/HuSnJ
000023   FL/1ReJ
000025   FL/4ReJ
003024   FVB.129P2(B6)-Fmr1tm1Cgr/J
002539   FVB.129P2-Abcb4tm1Bor/J
002935   FVB.129S2(B6)-Ccnd1tm1Wbg/J
002953   FVB.Cg-Tg(MMTVTGFA)254Rjc/J
003170   FVB.Cg-Tg(Myh6-tTA)6Smbf/J
003078   FVB.Cg-Tg(WapIgf1)39Dlr/J
003487   FVB.Cg-Tg(XGFAP-lacZ)3Mes/J
003257   FVB/N-Tg(GFAPGFP)14Mes/J
002856   FVB/N-Tg(TIE2-lacZ)182Sato/J
002384   FVB/N-Tg(UcpDta)1Kz/J
001800   FVB/NJ
001491   FVB/NMob
000804   HPG/BmJ
000734   MOLD/RkJ
000550   MOLF/EiJ
002423   NON/ShiLtJ
000679   P/J
000680   PL/J
000268   RSV/LeJ
000269   SB/LeJ
010968   SB;C3Sn-Lrp4mdig-2J/GrsrJ
005651   SJL.AK-Thy1a/TseJ
000686   SJL/J
000688   ST/bJ
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
002648   STOCK a/a Cln6nclf/J
000279   STOCK gr +/+ Ap3d1mh/J
005965   STOCK Tg(Pomc1-cre)16Lowl/J
004770   SW.B6-Soab/J
002023   SWR.M-Emv21 Emv22/J
000689   SWR/J
000939   SWR/J-Clcn1adr-mto/J
000692   WB/ReJ KitW/J
100410   WBB6F1/J-KitW/KitW-v/J
000693   WC/ReJ KitlSl/J
View Strains carrying   Pde6brd1     (73 strains)

Strains carrying other alleles of Fasl
014547   FVB/N-Tg(tetO-Fasl)BDepa/J
003499   NOD-Tg(Ins2-Fasl)24Ach/J
View Strains carrying other alleles of Fasl     (2 strains)

View Strains carrying other alleles of Pde6b     (15 strains)


Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- 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; ALPS
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Lung Cancer   (FASLG)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype


  • mortality/aging
  • *normal* mortality/aging
    • when placed under hyperoxic conditions for >5 days, mice do not show increased survival (resistance to hyperoxia) compared to wild-type mice   (MGI Ref ID J:120650)
    • premature death   (MGI Ref ID J:29572)
      • males survived to mean age of 396 days, females to 369 days, controls survived until 688 days   (MGI Ref ID J:7306)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • no defect detected: no vascular disease, including necrotizing arteritis or polyarteritis   (MGI Ref ID J:7306)
  • hematopoietic system phenotype
  • abnormal T cell differentiation
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:8267)
    • express beta-chain of TCR   (MGI Ref ID J:8267)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:8267)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:8267)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:8267)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:8267)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:12002)
    • express beta-chain of TCR   (MGI Ref ID J:12002)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:12002)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:12002)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:12002)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:12002)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:12002)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:12002)
  • anemia
    • evident in 40% of animals autopsied when moribund   (MGI Ref ID J:7306)
  • decreased B cell number
    • 36 to 15%   (MGI Ref ID J:29572)
  • decreased cytotoxic T cell cytolysis
    • in Fas-dependent lysis assays, but not allogeneic targets   (MGI Ref ID J:17698)
  • enlarged spleen
    • evident after 13 weeks of age   (MGI Ref ID J:7306)
    • 4-fold enlargement compared to controls   (MGI Ref ID J:29572)
  • increased immunoglobulin level
    • developed broad-based hypergammaglobulinemia   (MGI Ref ID J:29572)
    • development of broad-based hypergammaglobulinemia   (MGI Ref ID J:7306)
    • increased IgA level   (MGI Ref ID J:7306)
    • increased IgG level
      • 10-fold IgG2a   (MGI Ref ID J:29572)
      • 3- to 6-fold IgG1 and IgG2b   (MGI Ref ID J:29572)
      • increased IgG1 level   (MGI Ref ID J:7306)
      • increased IgG2a level   (MGI Ref ID J:7306)
      • increased IgG2b level   (MGI Ref ID J:7306)
    • increased IgM level   (MGI Ref ID J:29572)
  • increased leukocyte cell number   (MGI Ref ID J:7306)
    • increased lymphocyte cell number
      • 5-fold increase in peripheral blood lymphocytes   (MGI Ref ID J:29572)
      • 4-fold greater than controls   (MGI Ref ID J:7306)
      • increased T cell number
        • 59 to 68%   (MGI Ref ID J:29572)
    • increased neutrophil cell number
      • 2-fold greater than controls   (MGI Ref ID J:7306)
  • homeostasis/metabolism phenotype
  • skin edema
    • ~25% of those autopsied when moribund showed marked subcutaneous edema   (MGI Ref ID J:7306)
  • immune system phenotype
  • abnormal T cell differentiation
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:8267)
    • express beta-chain of TCR   (MGI Ref ID J:8267)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:8267)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:8267)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:8267)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:8267)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:12002)
    • express beta-chain of TCR   (MGI Ref ID J:12002)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:12002)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:12002)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:12002)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:12002)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:12002)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:12002)
  • abnormal lymph node morphology   (MGI Ref ID J:7306)
    • enlarged lymph nodes
      • 50-fold heavier at 20 weeks of age than controls   (MGI Ref ID J:29572)
      • enlarged peripheral lymph nodes evident at 13 weeks of age, abdominal evident shortly thereafter   (MGI Ref ID J:7306)
      • 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   (MGI Ref ID J:7306)
  • decreased B cell number
    • 36 to 15%   (MGI Ref ID J:29572)
  • decreased cytotoxic T cell cytolysis
    • in Fas-dependent lysis assays, but not allogeneic targets   (MGI Ref ID J:17698)
  • enlarged spleen
    • evident after 13 weeks of age   (MGI Ref ID J:7306)
    • 4-fold enlargement compared to controls   (MGI Ref ID J:29572)
  • increased autoantibody level
    • thymocyte-binding autoantibody present   (MGI Ref ID J:7306)
    • increased anti-nuclear antigen antibody level
      • high titers of antinuclear autoantibodies evident by 16 weeks of age in all mice assayed   (MGI Ref ID J:7306)
      • high titers of antinuclear autoantibodies evident at 14 weeks of age   (MGI Ref ID J:29572)
      • increased anti-double stranded DNA antibody level
        • high concentrations of anti-dsDNA autoantibodies present   (MGI Ref ID J:7306)
  • increased immunoglobulin level
    • developed broad-based hypergammaglobulinemia   (MGI Ref ID J:29572)
    • development of broad-based hypergammaglobulinemia   (MGI Ref ID J:7306)
    • increased IgA level   (MGI Ref ID J:7306)
    • increased IgG level
      • 10-fold IgG2a   (MGI Ref ID J:29572)
      • 3- to 6-fold IgG1 and IgG2b   (MGI Ref ID J:29572)
      • increased IgG1 level   (MGI Ref ID J:7306)
      • increased IgG2a level   (MGI Ref ID J:7306)
      • increased IgG2b level   (MGI Ref ID J:7306)
    • increased IgM level   (MGI Ref ID J:29572)
  • increased leukocyte cell number   (MGI Ref ID J:7306)
    • increased lymphocyte cell number
      • 5-fold increase in peripheral blood lymphocytes   (MGI Ref ID J:29572)
      • 4-fold greater than controls   (MGI Ref ID J:7306)
      • increased T cell number
        • 59 to 68%   (MGI Ref ID J:29572)
    • increased neutrophil cell number
      • 2-fold greater than controls   (MGI Ref ID J:7306)
  • interstitial pneumonia
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund   (MGI Ref ID J:7306)
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype
    • despite glomerular deposition of immune complexes, no, or very little, glomerulonephritis was observed   (MGI Ref ID J:7306)
  • respiratory system phenotype
  • interstitial pneumonia
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund   (MGI Ref ID J:7306)
  • tumorigenesis
  • *normal* tumorigenesis
    • regression of transplanted SCCVII tumors by gene therapy treatment with Il12b is normal   (MGI Ref ID J:108303)
  • integument phenotype
  • skin edema
    • ~25% of those autopsied when moribund showed marked subcutaneous edema   (MGI Ref ID J:7306)


  • hematopoietic system phenotype
  • abnormal T cell morphology
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-   (MGI Ref ID J:8267)
  • abnormal T cell physiology
    • cells do not generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • abnormal T cell proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (MGI Ref ID J:8267)
  • homeostasis/metabolism phenotype
  • abnormal interleukin level
    • stimulation with concanavalin A does not induce cells to produce Il2   (MGI Ref ID J:8267)
  • immune system phenotype
  • abnormal T cell morphology
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-   (MGI Ref ID J:8267)
  • abnormal T cell physiology
    • cells do not generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • abnormal T cell proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (MGI Ref ID J:8267)
  • abnormal interleukin level
    • stimulation with concanavalin A does not induce cells to produce Il2   (MGI Ref ID J:8267)
  • nervous system phenotype
  • decreased neuron apoptosis
    • 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   (MGI Ref ID J:124252)
    • neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death   (MGI Ref ID J:124252)
  • cellular phenotype
  • decreased neuron apoptosis
    • 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   (MGI Ref ID J:124252)
    • neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death   (MGI Ref ID J:124252)


        involves: C3H/HeJ
  • immune system phenotype
  • abnormal osteoclast physiology
    • 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture   (MGI Ref ID J:156947)
  • enlarged lymph nodes   (MGI Ref ID J:171440)
  • enlarged spleen   (MGI Ref ID J:171440)
    • increased spleen weight   (MGI Ref ID J:171440)
  • skeleton phenotype
  • abnormal osteoclast physiology
    • 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture   (MGI Ref ID J:156947)
  • hematopoietic system phenotype
  • abnormal osteoclast physiology
    • 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture   (MGI Ref ID J:156947)
  • enlarged spleen   (MGI Ref ID J:171440)
    • increased spleen weight   (MGI Ref ID J:171440)

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


  • 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)   (MGI Ref ID J:120427)
    • 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)   (MGI Ref ID J:120427)
      • tissue damage is less frequent at 45 days than in Prf-null mice   (MGI Ref ID J:120427)
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls   (MGI Ref ID J:120427)
  • abnormal NK cell physiology
    • continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver   (MGI Ref ID J:115033)
  • abnormal osteoclast physiology
    • osteoclasts are resistant to estrogen induced apoptosis   (MGI Ref ID J:127179)
  • 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   (MGI Ref ID J:136745)
  • eye inflammation
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction   (MGI Ref ID J:136745)
    • 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   (MGI Ref ID J:136745)
  • 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   (MGI Ref ID J:136745)
  • 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   (MGI Ref ID J:120427)
  • liver inflammation
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • reproductive system phenotype
  • abnormal sperm number
    • epididymal sperm count is increased compared to in wild-type mice due to decreased sperm apoptosis   (MGI Ref ID J:146994)
  • abnormal sperm physiology
    • sperm apoptosis is decreased compared to in wild-type mice   (MGI Ref ID J:146994)
  • 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   (MGI Ref ID J:135830)
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
  • focal hepatic necrosis
    • necroinflammatory foci after BDL are reduced in number compared to controls after BDL   (MGI Ref ID J:135830)
  • liver inflammation
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • 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   (MGI Ref ID J:136745)
  • eye inflammation
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction   (MGI Ref ID J:136745)
    • 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   (MGI Ref ID J:136745)
  • 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)   (MGI Ref ID J:120427)
    • 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)   (MGI Ref ID J:120427)
      • tissue damage is less frequent at 45 days than in Prf-null mice   (MGI Ref ID J:120427)
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls   (MGI Ref ID J:120427)
  • demyelination
    • at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice   (MGI Ref ID J:120427)
  • homeostasis/metabolism phenotype
  • decreased circulating alanine transaminase level
    • one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls   (MGI Ref ID J:135830)
  • hematopoietic system phenotype
  • abnormal NK cell physiology
    • continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver   (MGI Ref ID J:115033)
  • abnormal osteoclast physiology
    • osteoclasts are resistant to estrogen induced apoptosis   (MGI Ref ID J:127179)
  • 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   (MGI Ref ID J:136745)
  • skeleton phenotype
  • abnormal osteoclast physiology
    • osteoclasts are resistant to estrogen induced apoptosis   (MGI Ref ID J:127179)
  • cellular phenotype
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)


        involves: C3H/HeJ * CBA
  • reproductive system phenotype
  • *normal* 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 death   (MGI Ref ID J:114219)


        involves: C3H/HeJ * C57BL/6
  • mortality/aging
  • premature death   (MGI Ref ID J:153501)
  • immune system phenotype
  • *normal* immune system phenotype
    • mice mount a normal immune response to influenza   (MGI Ref ID J:153501)
    • dermatitis
      • in 10% of mice and later than in Fasltm1.1Ast homozygotes   (MGI Ref ID J:153501)
    • enlarged lymph nodes
    • enlarged spleen
    • increased IgE level   (MGI Ref ID J:153501)
    • increased IgG level   (MGI Ref ID J:153501)
      • increased IgG1 level   (MGI Ref ID J:153501)
      • increased IgG2a level   (MGI Ref ID J:153501)
      • increased IgG2b level   (MGI Ref ID J:153501)
    • increased T cell number
      • TCRalpha/beta+CD4-CD8-B220+ T cells   (MGI Ref ID J:153501)
    • increased anti-nuclear antigen antibody level
    • increased circulating tumor necrosis factor level   (MGI Ref ID J:153501)
    • increased susceptibility to systemic lupus erythematosus
      • by 57 weeks, 15% of mice develop fatal SLE-like autoimmune kidney disease unlike wild-type mice   (MGI Ref ID J:153501)
  • tumorigenesis
  • increased histiocytic sarcoma incidence
  • 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   (MGI Ref ID J:76811)
    • following pancreatic duct ligation, mice exhibit less acinar cell apoptosis than similarly treated wild-type mice   (MGI Ref ID J:76811)
    • however, areas of inflammation and fibrosis are sometimes observed following pancreatic duct ligation   (MGI Ref ID J:76811)
  • increased circulating tumor necrosis factor level   (MGI Ref ID J:153501)
  • hematopoietic system phenotype
  • enlarged spleen
  • increased IgE level   (MGI Ref ID J:153501)
  • increased IgG level   (MGI Ref ID J:153501)
    • increased IgG1 level   (MGI Ref ID J:153501)
    • increased IgG2a level   (MGI Ref ID J:153501)
    • increased IgG2b level   (MGI Ref ID J:153501)
  • increased T cell number
    • TCRalpha/beta+CD4-CD8-B220+ T cells   (MGI Ref ID J:153501)
  • integument phenotype
  • dermatitis
    • in 10% of mice and later than in Fasltm1.1Ast homozygotes   (MGI Ref ID J:153501)


  • immune system phenotype
  • abnormal lymph node morphology
    • mutants exhibit an increase in apoptotic material in the lymph nodes   (MGI Ref ID J:91058)
    • enlarged lymph nodes
      • increase in lymph node size and weight   (MGI Ref ID J:91058)
  • enlarged spleen   (MGI Ref ID J:91058)
    • increased spleen weight   (MGI Ref ID J:91058)
  • impaired macrophage phagocytosis
    • clearance of apoptotic material by macrophages is reduced   (MGI Ref ID J:91058)
    • mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice   (MGI Ref ID J:91058)
  • increased autoantibody level
    • serum levels of anticardiolipin antibody are modestly elevated on a normal diet and are further elevated on a Western diet   (MGI Ref ID J:91058)
    • increased anti-nuclear antigen antibody level
      • high titers of anti-nuclear antigen antibodies (ANAs) on normal and Western diet   (MGI Ref ID J:91058)
  • cellular phenotype
  • increased apoptosis
    • mutants exhibit an increase in apoptotic material in the lymph nodes   (MGI Ref ID J:91058)
  • hematopoietic system phenotype
  • enlarged spleen   (MGI Ref ID J:91058)
    • increased spleen weight   (MGI Ref ID J:91058)
  • impaired macrophage phagocytosis
    • clearance of apoptotic material by macrophages is reduced   (MGI Ref ID J:91058)
    • mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice   (MGI Ref ID J:91058)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • lipid levels are normal   (MGI Ref ID J:91058)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • mutants do not develop atherosclerotic lesions and do not show macrophage or T cell infiltration in the aorta   (MGI Ref ID J:91058)
View Research Applications

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

Faslgld related

Apoptosis Research
Extracellular Modulators

Cancer Research
Genes Regulating Growth and Proliferation

Cell Biology Research
Signal Transduction

Hematological Research

Immunology, Inflammation and Autoimmunity Research
      lupus erythematosus

Pde6brd1 related

Sensorineural Research
Retinal Degeneration

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Faslgld
Allele Name generalized lymphoproliferative disease
Allele Type Spontaneous
Common Name(s) CD95-; FasL-; Tnfsf6gld; gld;
Strain of OriginC3H/HeJ
Gene Symbol and Name Fasl, Fas ligand (TNF superfamily, member 6)
Chromosome 1
Gene Common Name(s) ALPS1B; APT1LG1; APTL; CD178; CD95-L; CD95L; Fas antigen ligand; Fas-L; TNFSF6; Tnfsf6; generalized lymphoproliferative disease; gld; tumor necrosis factor (ligand) superfamily, member 6;
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. [MGI Ref ID J:17445]
Allele Symbol Pde6brd1
Allele Name retinal degeneration 1
Allele Type Spontaneous
Common Name(s) Pdebrd1; rd; rd-1; rd1; rodless retina;
Strain of Originvarious
Gene Symbol and Name Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Chromosome 5
Gene Common Name(s) CSNB3; CSNBAD2; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10;
General Note The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
Molecular Note Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361]


Genotyping Information

Genotyping Protocols

Faslgld, Restriction Enzyme Digest

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:63433]

Additional References

Faslgld 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:85214]

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):11832-40. [PubMed: 11090183]  [MGI Ref ID J:65895]

Chattopadhyay G; Khan AQ; Sen G; Colino J; DuBois W; Rubtsov A; Torres RM; Potter M; Snapper CM. 2007. Transgenic expression of Bcl-xL or Bcl-2 by murine B cells enhances the in vivo antipolysaccharide, but not antiprotein, response to intact Streptococcus pneumoniae. J Immunol 179(11):7523-34. [PubMed: 18025197]  [MGI Ref ID J:154811]

Cheng LE; Chan FK; Cado D; Winoto A. 1997. Functional redundancy of the Nur77 and Nor-1 orphan steroid receptors in T-cell apoptosis. EMBO J 16(8):1865-75. [PubMed: 9155013]  [MGI Ref ID J:40025]

Chrobak P; Gress RE. 2001. Veto activity of activated bone marrow does not require perforin and Fas ligand. Cell Immunol 208(2):80-7. [PubMed: 11333140]  [MGI Ref ID J:127838]

Chu JL; Ramos P; Rosendorff A; Nikolic-Zugic J; Lacy E; Matsuzawa A; Elkon KB. 1995. Massive upregulation of the Fas ligand in lpr and gld mice: implications for Fas regulation and the graft-versus-host disease-like wasting syndrome. J Exp Med 181(1):393-8. [PubMed: 7528774]  [MGI Ref ID J:22200]

Chung CS; Wang W; Chaudry IH; Ayala A. 2001. Increased apoptosis in lamina propria B cells during polymicrobial sepsis is FasL but not endotoxin mediated. Am J Physiol Gastrointest Liver Physiol 280(5):G812-8. [PubMed: 11292588]  [MGI Ref ID J:69305]

Coerver KA; Woodruff TK; Finegold MJ; Mather J; Bradley A; Matzuk MM. 1996. Activin signaling through activin receptor type II causes the cachexia-like symptoms in inhibin-deficient mice. Mol Endocrinol 10(5):534-43. [PubMed: 8732684]  [MGI Ref ID J:112001]

Cohen PL; Eisenberg RA. 1991. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease. Annu Rev Immunol 9:243-69. [PubMed: 1910678]  [MGI Ref ID J:27579]

Cohen PL; Eisenberg RA. 1992. The lpr and gld genes in systemic autoimmunity: life and death in the Fas lane [published erratum appears in Immunol Today 1993 Feb;14(2):97] Immunol Today 13(11):427-8. [PubMed: 1282318]  [MGI Ref ID J:3363]

Colino J; Snapper CM. 2003. Two distinct mechanisms for induction of dendritic cell apoptosis in response to intact Streptococcus pneumoniae. J Immunol 171(5):2354-65. [PubMed: 12928382]  [MGI Ref ID J:121185]

Conceicao-Silva F; Hahne M; Schroter M; Louis J; Tschopp J. 1998. The resolution of lesions induced by Leishmania major in mice requires a functional Fas (APO-1, CD95) pathway of cytotoxicity Eur J Immunol 28(1):237-45. [PubMed: 9485203]  [MGI Ref ID J:45903]

Cone RE; Li X; Sharafieh R; O'Rourke J; Vella AT. 2007. The suppression of delayed-type hypersensitivity by CD8+ regulatory T cells requires interferon-gamma. Immunology 120(1):112-9. [PubMed: 17052246]  [MGI Ref ID J:122316]

Couillard M; Guillaume R; Tanji N; D'Agati V; Trudel M. 2002. c-myc-induced apoptosis in polycystic kidney disease is independent of FasL/Fas interaction. Cancer Res 62(8):2210-4. [PubMed: 11956070]  [MGI Ref ID J:134937]

Crawford HC; Scoggins CR; Washington MK; Matrisian LM; Leach SD. 2002. Matrix metalloproteinase-7 is expressed by pancreatic cancer precursors and regulates acinar-to-ductal metaplasia in exocrine pancreas. J Clin Invest 109(11):1437-44. [PubMed: 12045257]  [MGI Ref ID J:76811]

Cretney E; Uldrich AP; McNab FW; Godfrey DI; Smyth MJ. 2008. No requirement for TRAIL in intrathymic negative selection. Int Immunol 20(2):267-76. [PubMed: 18192669]  [MGI Ref ID J:131293]

Cullen CM; Bonventre PF; Heeg H; Bluethmann H; Mountz JD; Edwards CK 3rd. 1995. A fas antigen receptor mutation allows development of toxic shock syndrome toxin-1-induced lethal shock in V beta 8.2 T-cell receptor transgenic mice. Pathobiology 63(6):293-304. [PubMed: 8738468]  [MGI Ref ID J:33149]

Dakhova O; O'Day D; Kinet N; Yucer N; Wiese M; Shetty G; Ducy P. 2009. Dickkopf-like1 regulates postpubertal spermatocyte apoptosis and testosterone production. Endocrinology 150(1):404-12. [PubMed: 18818293]  [MGI Ref ID J:146994]

Dautigny N; Le Campion A; Lucas B. 1999. Timing and casting for actors of thymic negative selection. J Immunol 162(3):1294-302. [PubMed: 9973382]  [MGI Ref ID J:124433]

Davidson WF; Dumont FJ; Bedigian HG; Fowlkes BJ; Morse HC 3rd. 1986. Phenotypic, functional, and molecular genetic comparisons of the abnormal lymphoid cells of C3H-lpr/lpr and C3H-gld/gld mice. J Immunol 136(11):4075-84. [PubMed: 3009614]  [MGI Ref ID J:8267]

Davidson WF; Holmes KL; Roths JB; Morse HC 3rd. 1985. Immunologic abnormalities of mice bearing the gld mutation suggest a common pathway for murine nonmalignant lymphoproliferative disorders with autoimmunity. Proc Natl Acad Sci U S A 82(4):1219-23. [PubMed: 3856256]  [MGI Ref ID J:12002]

Davies MH; Eubanks JP; Powers MR. 2003. Increased retinal neovascularization in Fas ligand-deficient mice. Invest Ophthalmol Vis Sci 44(7):3202-10. [PubMed: 12824272]  [MGI Ref ID J:117984]

Desbarats J; Newell MK. 2000. Fas engagement accelerates liver regeneration after partial hepatectomy. Nat Med 6(8):920-3. [PubMed: 10932231]  [MGI Ref ID J:118048]

Dittel BN; Merchant RM; Janeway CA Jr. 1999. Evidence for Fas-dependent and Fas-independent mechanisms in the pathogenesis of experimental autoimmune encephalomyelitis. J Immunol 162(11):6392-400. [PubMed: 10352252]  [MGI Ref ID J:110922]

Dix RD; Podack ER; Cousins SW. 2003. Loss of the perforin cytotoxic pathway predisposes mice to experimental cytomegalovirus retinitis. J Virol 77(6):3402-8. [PubMed: 12610115]  [MGI Ref ID J:82226]

Dudani R; Russell M; van Faassen H; Krishnan L; Sad S. 2008. Mutation in the Fas Pathway Impairs CD8+ T Cell Memory. J Immunol 180(5):2933-41. [PubMed: 18292515]  [MGI Ref ID J:131560]

Edinger M; Hoffmann P; Ermann J; Drago K; Fathman CG; Strober S; Negrin RS. 2003. CD4+CD25+ regulatory T cells preserve graft-versus-tumor activity while inhibiting graft-versus-host disease after bone marrow transplantation. Nat Med 9(9):1144-50. [PubMed: 12925844]  [MGI Ref ID J:126172]

Eisenberg RA; Sobel ES; Reap EA; Halpern MD; Cohen PL. 1994. The role of B cell abnormalities in the systemic autoimmune syndromes of lpr and gld mice. Semin Immunol 6(1):49-54. [PubMed: 8167307]  [MGI Ref ID J:19055]

Embree-Ku M; Boekelheide K. 2002. Absence of p53 and FasL has sexually dimorphic effects on both development and reproduction. Exp Biol Med (Maywood) 227(7):545-53. [PubMed: 12094020]  [MGI Ref ID J:103281]

Embree-Ku M; Boekelheide K. 2002. FasL deficiency enhances the development of tumors in p53+/- mice. Toxicol Pathol 30(6):705-13. [PubMed: 12512872]  [MGI Ref ID J:81060]

Engelbert M; Gilmore MS. 2005. Fas ligand but not complement is critical for control of experimental Staphylococcus aureus Endophthalmitis. Invest Ophthalmol Vis Sci 46(7):2479-86. [PubMed: 15980239]  [MGI Ref ID J:136745]

Ettinger R; Wang JK; Bossu P; Papas K; Sidman CL; Abbas AK; Marshak-Rothstein A. 1994. Functional distinctions between MRL-lpr and MRL-gld lymphocytes. Normal cells reverse the gld but not lpr immunoregulatory defect. J Immunol 152(4):1557-68. [PubMed: 8120369]  [MGI Ref ID J:16936]

Fan H; Patel VA; Longacre A; Levine JS. 2006. Abnormal regulation of the cytoskeletal regulator Rho typifies macrophages of the major murine models of spontaneous autoimmunity. J Leukoc Biol 79(1):155-65. [PubMed: 16244106]  [MGI Ref ID J:104741]

Fecho K; Bentley SA; Cohen PL. 1998. Mice deficient in fas ligand (gld) or fas (lpr) show few alterations in granulopoiesis. Cell Immunol 188(1):19-32. [PubMed: 9743554]  [MGI Ref ID J:50037]

Fields ML; Nish SA; Hondowicz BD; Metzgar MH; Wharton GN; Caton AJ; Erikson J. 2005. The influence of effector T cells and Fas ligand on lupus-associated B cells. J Immunol 175(1):104-11. [PubMed: 15972636]  [MGI Ref ID J:100620]

Fields ML; Sokol CL; Eaton-Bassiri A; Seo Sj; Madaio MP; Erikson J. 2001. Fas/fas ligand deficiency results in altered localization of anti-double-stranded dna b cells and dendritic cells. J Immunol 167(4):2370-8. [PubMed: 11490027]  [MGI Ref ID J:70822]

Fingleton B; Carter KJ; Matrisian LM. 2007. Loss of functional Fas ligand enhances intestinal tumorigenesis in the Min mouse model. Cancer Res 67(10):4800-6. [PubMed: 17510409]  [MGI Ref ID J:121728]

Fogler WE; Volker K; Watanabe M; Wigginton JM; Roessler P; Brunda MJ; Ortaldo JR; Wiltrout RH. 1998. Recruitment of hepatic NK cells by IL-12 is dependent on IFN-gamma and VCAM-1 and is rapidly down-regulated by a mechanism involving T cells and expression of Fas. J Immunol 161(11):6014-21. [PubMed: 9834083]  [MGI Ref ID J:115033]

Ford MS; Young KJ; Zhang Z; Ohashi PS; Zhang L. 2002. The immune regulatory function of lymphoproliferative double negative T cells in vitro and in vivo. J Exp Med 196(2):261-7. [PubMed: 12119351]  [MGI Ref ID J:120698]

Fraszczak J; Trad M; Janikashvili N; Cathelin D; Lakomy D; Granci V; Morizot A; Audia S; Micheau O; Lagrost L; Katsanis E; Solary E; Larmonier N; Bonnotte B. 2010. Peroxynitrite-dependent killing of cancer cells and presentation of released tumor antigens by activated dendritic cells. J Immunol 184(4):1876-84. [PubMed: 20089706]  [MGI Ref ID J:159469]

Froidevaux S; Kuntz L; Velin D; Loor F. 1991. Different nature of the proliferation defects of GLD, LPR and MEV C57BL/6 mouse lymphoid cells. Autoimmunity 10(3):233-40. [PubMed: 1756226]  [MGI Ref ID J:1661]

Froidevaux S; Rosenblatt N; Loor F. 1992. Adoptive transfer of the generalized lymphoproliferative disease (gld) syndrome in nude beige mice. Immunology 75(4):693-9. [PubMed: 1592442]  [MGI Ref ID J:581]

Fujikura D; Chiba S; Muramatsu D; Kazumata M; Nakayama Y; Kawai T; Akira S; Kida H; Miyazaki T. 2013. Type-I interferon is critical for FasL expression on lung cells to determine the severity of influenza. PLoS One 8(2):e55321. [PubMed: 23408968]  [MGI Ref ID J:197206]

Fullerton AM; Roth RA; Ganey PE. 2013. 2,3,7,8-TCDD enhances the sensitivity of mice to concanavalin A immune-mediated liver injury. Toxicol Appl Pharmacol 266(2):317-27. [PubMed: 23164664]  [MGI Ref ID J:193201]

Giese T; Davidson WF. 1992. Evidence for early onset, polyclonal activation of T cell subsets in mice homozygous for lpr. J Immunol 149(9):3097-106. [PubMed: 1383337]  [MGI Ref ID J:3035]

Giese T; Davidson WF. 1995. The accumulation of B220+ CD4- CD8- (DN) T cells in C3H-lpr/lpr mice is not accelerated by the stimulation of CD8+ T cells or B220+ DN T cells with staphylococcal enterotoxin B and occurs independently of V beta 8+ T cells. Int Immunol 7(8):1213-23. [PubMed: 7495728]  [MGI Ref ID J:28207]

Graubert TA; DiPersio JF; Russell JH; Ley TJ. 1997. Perforin/granzyme-dependent and independent mechanisms are both important for the development of graft-versus-host disease after murine bone marrow transplantation. J Clin Invest 100(4):904-11. [PubMed: 9259590]  [MGI Ref ID J:42355]

Gregory MS; Hackett CG; Abernathy EF; Lee KS; Saff RR; Hohlbaum AM; Moody KS; Hobson MW; Jones A; Kolovou P; Karray S; Giani A; John SW; Chen DF; Marshak-Rothstein A; Ksander BR. 2011. Opposing roles for membrane bound and soluble fas ligand in glaucoma-associated retinal ganglion cell death. PLoS One 6(3):e17659. [PubMed: 21479271]  [MGI Ref ID J:171440]

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Thompson CL; Selby CP; Partch CL; Plante DT; Thresher RJ; Araujo F; Sancar A. 2004. Further evidence for the role of cryptochromes in retinohypothalamic photoreception/phototransduction. Brain Res Mol Brain Res 122(2):158-66. [PubMed: 15010208]  [MGI Ref ID J:88468]

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Thompson S; Stasheff SF; Hernandez J; Nylen E; East JS; Kardon RH; Pinto LH; Mullins RF; Stone EM. 2011. Different inner retinal pathways mediate rod-cone input in irradiance detection for the pupillary light reflex and regulation of behavioral state in mice. Invest Ophthalmol Vis Sci 52(1):618-23. [PubMed: 20847113]  [MGI Ref ID J:171559]

Thyagarajan S; van Wyk M; Lehmann K; Lowel S; Feng G; Wassle H. 2010. Visual function in mice with photoreceptor degeneration and transgenic expression of channelrhodopsin 2 in ganglion cells. J Neurosci 30(26):8745-58. [PubMed: 20592196]  [MGI Ref ID J:161847]

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Tu DC; Zhang D; Demas J; Slutsky EB; Provencio I; Holy TE; Van Gelder RN. 2005. Physiologic diversity and development of intrinsically photosensitive retinal ganglion cells. Neuron 48(6):987-99. [PubMed: 16364902]  [MGI Ref ID J:107606]

Tucker B; Klassen H; Yang L; Chen DF; Young MJ. 2008. Elevated MMP Expression in the MRL Mouse Retina Creates a Permissive Environment for Retinal Regeneration. Invest Ophthalmol Vis Sci 49(4):1686-95. [PubMed: 18385092]  [MGI Ref ID J:136153]

Usui S; Oveson BC; Lee SY; Jo YJ; Yoshida T; Miki A; Miki K; Iwase T; Lu L; Campochiaro PA. 2009. NADPH oxidase plays a central role in cone cell death in retinitis pigmentosa. J Neurochem 110(3):1028-37. [PubMed: 19493169]  [MGI Ref ID J:152819]

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Vazquez-Chona FR; Clark AM; Levine EM. 2009. Rlbp1 promoter drives robust Muller glial GFP expression in transgenic mice. Invest Ophthalmol Vis Sci 50(8):3996-4003. [PubMed: 19324864]  [MGI Ref ID J:154561]

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Yamada H; Yamada E; Hackett SF; Ozaki H; Okamoto N; Campochiaro PA. 1999. Hyperoxia causes decreased expression of vascular endothelial growth factor and endothelial cell apoptosis in adult retina. J Cell Physiol 179(2):149-56. [PubMed: 10199554]  [MGI Ref ID J:54326]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

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Pricing for USA, Canada and Mexico shipping destinations View International Pricing


Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2625.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing


Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3412.50
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

   000659 C3H/HeJ
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.

Important Note

This strain is homozygous for the retinal degeneration allele Pde6brd1.

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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The Jackson Laboratory's Genotype Promise

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.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

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In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.