Strain Name:

B6Smn.C3-Faslgld/J

Stock Number:

001021

Availability:

Level 4

Description

Strain Information

Former Names B6Smn.C3-Tnfsf6gld/J    (Changed: 14-MAR-05 )
Type Congenic; Mutant Strain; Spontaneous Mutation;
Mating SystemHomozygote x Homozygote         (Female x Male)
Specieslaboratory mouse
Background Strain C57BL/6Smn
Donor Strain C3H/HeJ-Tnfsf6gld
H2 Haplotypeb
GenerationN10F19+58 (11-JAN-08)

Appearance
black
Related Genotype: a/a

Description
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. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

The Cryaalop18 mutation was identified in the C57BL/6JSmn inbred strain in approximately 1991. This is at least 5 years from the date of the final (N10) backcross generation of B6Smn.C3-Faslgld/J. In 2003, four B6Smn.C3-Faslgld/J mice were assessed and the recessive lop18 phenotype was absent from all of them. This does not guarantee that the Cryaalop18 mutation is absent from this strain.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Faslgld allele
000784   C3H/HeJ-Faslgld/J
002932   CPt.C3-Faslgld/J
008223   NOD.C3(B6)-Faslgld /LwnJ
View Strains carrying   Faslgld     (3 strains)

Strains carrying other alleles of Fasl
003499   NOD-Tg(Ins2-Fasl)24Ach
View Strains carrying other alleles of Fasl     (1 strain)

Additional Web Information

Congenic Nomenclature
Genetic Quality Control Annual Report

Phenotype

Phenotype Information

Related Disease (OMIM) Terms

Autoimmune Lymphoproliferative Syndrome; ALPS

Mammalian Phenotype Terms assigned by genotype

Faslgld/Faslgld

        B6Smn.C3-Faslgld/J
  • nervous system phenotype
  • CNS inflammation (MGI Ref ID J:120427)
    • 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 (MGI Ref ID J:120427)
      • 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
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
  • demyelination (MGI Ref ID J:120427)
    • at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice
  • immune system phenotype
  • CNS inflammation (MGI Ref ID J:120427)
    • 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 (MGI Ref ID J:120427)
      • 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
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
  • abnormal osteoclast physiology (MGI Ref ID J:127179)
    • osteoclasts are resistant to estrogen induced apoptosis
  • decreased granulocyte number (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
  • eye inflammation (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
  • increased susceptibility to bacterial infection (MGI Ref ID J:136745)
    • 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 (MGI Ref ID J:120427)
    • inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days
  • liver inflammation (MGI Ref ID J:135830)
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls
  • skeleton phenotype
  • abnormal osteoclast physiology (MGI Ref ID J:127179)
    • osteoclasts are resistant to estrogen induced apoptosis
  • decreased bone density (MGI Ref ID J:127179)
    • female mice do not lose bone density when ovaries are removed
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:136745)
    • 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 (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection
  • hematopoietic system phenotype
  • decreased granulocyte number (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
  • homeostasis/metabolism phenotype
  • decreased circulating alanine transaminase level (MGI Ref ID J:135830)
    • one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology (MGI Ref ID J:135830)
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL
    • decreased hepatocyte apoptosis (MGI Ref ID J:135830)
      • hepatocyte cell death is reduced compared to controls after BDL
  • focal hepatic necrosis (MGI Ref ID J:135830)
    • necroinflammatory foci after BDL are reduced in number compared to controls after BDL
  • liver inflammation (MGI Ref ID J:135830)
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Faslgld/Faslgld

        C3H/HeJ-Faslgld/J
  • life span-post-weaning/aging
  • *normal* life span-post-weaning/aging (MGI Ref ID J:120650)
    • when placed under hyperoxic conditions for >5 days, mice do not show increased survival (resistance to hyperoxia) compared to wild-type mice
    • premature death (MGI Ref ID J:29572)
      • males survived to mean age of 396 days, females to 369 days, controls survived until 688 days
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype (MGI Ref ID J:7306)
    • no defect detected: no vascular disease, including necrotizing arteritis or polyarteritis
  • hematopoietic system phenotype
  • abnormal T cell differentiation (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
  • anemia (MGI Ref ID J:7306)
    • evident in 40% of animals autopsied when moribund
  • decreased B cell number (MGI Ref ID J:29572)
    • 36 to 15%
  • enlarged spleen (MGI Ref ID J:7306)
    • evident after 13 weeks of age
    • 4-fold enlargement compared to controls
  • increased leukocyte cell number (MGI Ref ID J:7306)
    • increased lymphocyte cell number (MGI Ref ID J:29572)
      • 5-fold increase in peripheral blood lymphocytes
      • 4-fold greater than controls
      • increased T cell number (MGI Ref ID J:29572)
        • 59 to 68%
    • increased neutrophil cell number (MGI Ref ID J:7306)
      • 2-fold greater than controls
  • homeostasis/metabolism phenotype
  • skin edema (MGI Ref ID J:7306)
    • ~25% of those autopsied when moribund showed marked subcutaneous edema
  • immune system phenotype
  • abnormal T cell differentiation (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
    • express beta-chain of TCR
    • exhibit rearrangements of beta-chain genes
    • express TCR beta and alpha gene mRNA
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+
    • bind at high levels lectins that normally bind preferentially to B cells
    • did not proliferate or generate CTL in response to stimulation with alloantigens
    • cells stimulated with Con A failed to produce IL-2
  • abnormal lymph node morphology (MGI Ref ID J:7306)
    • enlarged lymph nodes (MGI Ref ID J:29572)
      • 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
  • decreased B cell number (MGI Ref ID J:29572)
    • 36 to 15%
  • defective cytotoxic T cell cytolysis (MGI Ref ID J:17698)
    • in Fas-dependent lysis assays, but not allogeneic targets
  • enlarged spleen (MGI Ref ID J:7306)
    • evident after 13 weeks of age
    • 4-fold enlargement compared to controls
  • increased autoantibody level (MGI Ref ID J:7306)
    • thymocyte-binding autoantibody present
    • increased anti-nuclear antigen antibody level (MGI Ref ID J:7306)
      • high titers of antinuclear autoantibodies evident by 16 weeks of age in all mice assayed
      • high titers of antinuclear autoantibodies evident at 14 weeks of age
      • increased anti-double stranded DNA antibody level (MGI Ref ID J:7306)
        • high concentrations of anti-dsDNA autoantibodies present
  • increased immunoglobulin level (MGI Ref ID J:29572)
    • developed broad-based hypergammaglobulinemia
    • development of broad-based hypergammaglobulinemia
    • increased IgA level (MGI Ref ID J:7306)
      • 10-fold
    • increased IgG level (MGI Ref ID J:29572)
      • 10-fold IgG2a
      • 3- to 6-fold IgG1 and IgG2b
      • 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 (MGI Ref ID J:29572)
      • 5-fold increase in peripheral blood lymphocytes
      • 4-fold greater than controls
      • increased T cell number (MGI Ref ID J:29572)
        • 59 to 68%
    • increased neutrophil cell number (MGI Ref ID J:7306)
      • 2-fold greater than controls
  • interstitial pneumonia (MGI Ref ID J:7306)
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype (MGI Ref ID J:7306)
    • despite glomerular deposition of immune complexes, no, or very little, glomerulonephritis was observed
  • respiratory system phenotype
  • interstitial pneumonia (MGI Ref ID J:7306)
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund
  • skin/coat/nails phenotype
  • skin edema (MGI Ref ID J:7306)
    • ~25% of those autopsied when moribund showed marked subcutaneous edema
  • tumorigenesis
  • *normal* tumorigenesis (MGI Ref ID J:108303)
    • regression of transplanted SCCVII tumors by gene therapy treatment with Il12b is normal

Faslgld/Faslgld

        C3H/HeJ-Faslgld
  • hematopoietic system phenotype
  • abnormal T cell morphology (MGI Ref ID J:8267)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • homeostasis/metabolism phenotype
  • abnormal interleukin level (MGI Ref ID J:8267)
    • stimulation with concanavalin A does not induce cells to produce Il2
  • immune system phenotype
  • abnormal T cell morphology (MGI Ref ID J:8267)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • abnormal T cell physiology (MGI Ref ID J:8267)
    • cells do not generate CTL in response to stimulation with alloantigens
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • abnormal interleukin level (MGI Ref ID J:8267)
    • stimulation with concanavalin A does not induce cells to produce Il2
  • nervous system phenotype
  • decreased neuron apoptosis (MGI Ref ID J:124252)
    • 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
    • neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death

Faslgld/Faslgld

        involves: C3H/HeJ * CBA
  • reproductive system phenotype
  • *normal* reproductive system phenotype (MGI Ref ID J:114219)
    • 2 days after gonadectomy, vaginal organ weight decreases by similar value as observed in wild-type, indicating normal estrogen-dependent cell death

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 and Inflammation Research
Autoimmunity (lupus erythematosus)

Mouse/Human Gene Homologs
systemic lupus erythematosus

Genes & Alleles

Gene & Allele Information

Allele Symbol Faslgld
Allele Name generalized lymphoproliferative disease
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) APT1LG1; CD178; 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]

Genotyping

Genotyping Information

Genotyping Protocols

Faslgld, REST, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Selected Reference(s)

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]

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]

Medana I; Li Z; Flugel A; Tschopp J; Wekerle H; Neumann H. 2001. Fas ligand (CD95L) protects neurons against perforin-mediated T lymphocyte cytotoxicity. J Immunol 167(2):674-81. [PubMed: 11441070]  [MGI Ref ID J:109872]

Riera L; Gariglio M; Pagano M; Gaiola O; Simon MM; Landolfo S. 2001. Control of murine cytomegalovirus replication in salivary glands during acute infection is independent of the Fas ligand/Fas system. New Microbiol 24(3):231-8. [PubMed: 11497079]  [MGI Ref ID J:109866]

Roths JB; Murphy ED; Eicher EM. 1984. A new mutation, gld, that produces lymphoproliferation and autoimmunity in C3H/HeJ mice. J Exp Med 159(1):1-20. [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]

Wigginton JM; Lee JK; Wiltrout TA; Alvord WG; Hixon JA; Subleski J; Back TC; Wiltrout RH. 2002. Synergistic engagement of an ineffective endogenous anti-tumor immune response and induction of IFN-gamma and Fas-ligand-dependent tumor eradication by combined administration of IL-18 and IL-2. J Immunol 169(8):4467-74. [PubMed: 12370382]  [MGI Ref ID J:109850]

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

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]

Dalton JE; Howell G; Pearson J; Scott P; Carding SR. 2004. Fas-Fas ligand interactions are essential for the binding to and killing of activated macrophages by gammadelta T cells. J Immunol 173(6):3660-7. [PubMed: 15356111]  [MGI Ref ID J:92754]

Gorbachev AV; Fairchild RL. 2004. CD4(+) T cells regulate CD8(+) T cell-mediated cutaneous immune responses by restricting effector T cell development through a Fas ligand-dependent mechanism. J Immunol 172(4):2286-95. [PubMed: 14764697]  [MGI Ref ID J:88048]

Hawes NL; Chang B; Hageman GS; Nusinowitz S; Nishina PM; Schneider BS; Smith RS; Roderick TH; Davisson MT; Heckenlively JR. 2000. Retinal degeneration 6 (rd6): a new mouse model for human retinitis punctata albescens. Invest Ophthalmol Vis Sci 41(10):3149-57. [PubMed: 10967077]  [MGI Ref ID J:64087]

Hori J; Joyce NC; Streilein JW. 2000. Immune privilege and immunogenicity reside among different layers of the mouse cornea. Invest Ophthalmol Vis Sci 41(10):3032-42. [PubMed: 10967061]  [MGI Ref ID J:64197]

Ma Y; Liu H; Tu-Rapp H; Thiesen HJ; Ibrahim SM; Cole SM; Pope RM. 2004. Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation. Nat Immunol 5(4):380-7. [PubMed: 15004557]  [MGI Ref ID J:89208]

Takeda K; Hayakawa Y; Van Kaer L; Matsuda H; Yagita H; Okumura K. 2000. Critical contribution of liver natural killer T cells to a murine model of hepatitis. Proc Natl Acad Sci U S A 97(10):5498-503. [PubMed: 10792025]  [MGI Ref ID J:62215]

Faslgld related

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]

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]

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