Strain Name:

B6.MRL-Faslpr/J

Stock Number:

000482

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Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. These mice serve as a model for systemic lupus erythematosus-like autoimmune syndromes.

Description

Strain Information

Former Names B6.MRL-Tnfrsf6lpr/J    (Changed: 26-JAN-05 )
Type Congenic; Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain MRL/MpJ-Faslpr
H2 Haplotypeb
GenerationN12F108 (05-AUG-14)
Generation Definitions

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Related Genotype: a/a

Description
Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr (Kelley and Roths 1985). Spontaneous production of anti-dsDNA autoantibodies is likewise affected with percentage binding of radiolabeled dsDNA in Faslpr/Faslpr mice varying from 5 percent on C57BL/6J to 26 percent on C3H/HeJ to as high as 49 percent on MRL/Mp (Izui et al 1984). Female MRL/Mp-Faslpr mice die at an average age of 17 weeks of age and males at 22 weeks. This compares to between 42 and 52 weeks in females on the C57BL/6J or C3H/HeJ background (Roths 1987). This mouse is a model for systemic lupus erythematosus-like autoimmune syndromes.

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.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Faslpr allele
000480   C3.MRL-Faslpr/J
002455   MRL.Cg-B2mtm1Unc Faslpr
022350   MRL.Cg-Nos2tm1Lau Faslpr/J
022760   MRL.Cg-Nos3tm1Unc Faslpr/J
003896   MRL/MpJ Faslpr-Foxq1sa-J/J
006825   MRL/MpJ-Faslpr/2J
000485   MRL/MpJ-Faslpr/J
004519   NOD.MRL(C3)-Faslpr/DoiJ
004922   NOD.MRL-Faslpr/Dvs
View Strains carrying   Faslpr     (9 strains)

Strains carrying other alleles of Fas
003233   B6.129P2-Fastm1Osa/J
007895   C57BL/6-Fastm1Cgn/J
001876   CBA/KlJms-Faslpr-cg/J
003234   MRL.129P2(B6)-Fastm1Osa/J
002983   MRL.CBAJms-Faslpr-cg/J
View Strains carrying other alleles of Fas     (5 strains)

Phenotype

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
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Systemic Lupus Erythematosus; SLE
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Sjogren Syndrome
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Faslpr/Faslpr

        B6.MRL-Faslpr/J
  • immune system phenotype
  • CNS inflammation   (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)
  • 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 splenic cell ratio
    • T1:follicular B cell ratio is higher than wild-type or Bcl2l11-deficient mice   (MGI Ref ID J:132217)
  • decreased B cell apoptosis
    • after bile duct ligation (BDL), Peyer's patch B cells do not display evidence of apoptosis   (MGI Ref ID J:135830)
  • enlarged lymph nodes
    • mice develop less severe lymphadenopathy at later ages than the double mutant Igh-6/Fas mice   (MGI Ref ID J:119584)
    • lymph node hyperplasia
      • total number of cells per lymph node is increased compared to wild-type   (MGI Ref ID J:132217)
  • increased autoantibody level
    • total anti-IgM antibody levels are increased compared to wild-type   (MGI Ref ID J:132217)
    • increased anti-nuclear antigen antibody level
      • anti-nuclear antibodies are increased compared to wild-type   (MGI Ref ID J:132217)
      • increased anti-double stranded DNA antibody level
        • anti-ssDNA IgM and IgG antibodies are increased compared to wild-type   (MGI Ref ID J:132217)
      • increased anti-histone antibody level
        • increased compared to wild-type   (MGI Ref ID J:132217)
      • increased anti-single stranded DNA antibody level
        • anti-ssDNA IgM and IgG antibodies are increased compared to wild-type   (MGI Ref ID J:132217)
  • increased follicular B cell number
    • higher in spleen relative to wild-type   (MGI Ref ID J:132217)
  • increased immature B cell number
    • plasmablast numbers in spleen are increased relative to wild-type   (MGI Ref ID J:132217)
    • increased transitional stage B cell number
      • higher numbers of T2 B cells in spleen relative to wild-type   (MGI Ref ID J:132217)
  • increased marginal zone B cell number
    • higher in spleen relative to wild-type, Faslpr homozygotes, and Bcl2l11-deficient mice   (MGI Ref ID J:132217)
  • increased splenocyte number
    • total number of CD19+ splenocytes is higher than wild-type   (MGI Ref ID J:132217)
    • total number of splenocytes is increased relative to wild-type   (MGI Ref ID J:132217)
  • 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, but lower counts than infected Faslgld 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)
  • 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 splenic cell ratio
    • T1:follicular B cell ratio is higher than wild-type or Bcl2l11-deficient mice   (MGI Ref ID J:132217)
  • decreased B cell apoptosis
    • after bile duct ligation (BDL), Peyer's patch B cells do not display evidence of apoptosis   (MGI Ref ID J:135830)
  • increased follicular B cell number
    • higher in spleen relative to wild-type   (MGI Ref ID J:132217)
  • increased immature B cell number
    • plasmablast numbers in spleen are increased relative to wild-type   (MGI Ref ID J:132217)
    • increased transitional stage B cell number
      • higher numbers of T2 B cells in spleen relative to wild-type   (MGI Ref ID J:132217)
  • increased marginal zone B cell number
    • higher in spleen relative to wild-type, Faslpr homozygotes, and Bcl2l11-deficient mice   (MGI Ref ID J:132217)
  • increased splenocyte number
    • total number of CD19+ splenocytes is higher than wild-type   (MGI Ref ID J:132217)
    • total number of splenocytes is increased relative to wild-type   (MGI Ref ID J:132217)
  • renal/urinary system phenotype
  • abnormal kidney morphology
    • number of macrophages surrounding glomeruli is increased compared to wild-type which have no macrophage index   (MGI Ref ID J:132217)
    • abnormal renal glomerulus basement membrane morphology
      • IgG deposits mainly localized to glomerular basement membrane are increased relative to wild-type   (MGI Ref ID J:132217)
  • increased renal glomerulus apoptosis
    • higher numbers of apoptotic cells are detected in glomeruli compared to wild-type   (MGI Ref ID J:132217)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls hours after BDL   (MGI Ref ID J:135830)
  • abnormal liver physiology
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
    • when mice are recipients of wild-type hepatitis B surface antigen (HBsAg)-specific Th1 cells after treatment with HBsAg, severe liver injury is induced to similar extent as in wild-type mice   (MGI Ref ID J:120559)
    • treatment with Prf1-deficient HBsAg-specific Th1 cells and HBsAg induces liver injury as severe as that induced by wild-type HBsAg-specific Th1 cells   (MGI Ref ID J:120559)
    • 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   (MGI Ref ID J:135830)
  • nervous system phenotype
  • CNS inflammation   (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)
  • demyelination
    • by 7 days after TMEV infection, inflammation is present in the meninges and gray matter of spinal cord, but decreases by 21 days, although not as much as in controls (B6)   (MGI Ref ID J:120427)
  • cellular phenotype
  • decreased B cell apoptosis
    • after bile duct ligation (BDL), Peyer's patch B cells do not display evidence of apoptosis   (MGI Ref ID J:135830)
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
  • increased renal glomerulus apoptosis
    • higher numbers of apoptotic cells are detected in glomeruli compared to wild-type   (MGI Ref ID J:132217)

Faslpr/Faslpr

        B6.MRL-Faslpr
  • mortality/aging
  • premature death
    • median survival is 284 days, compared to 795 days for controls   (MGI Ref ID J:6638)
    • 50% mortality is observed at 13.5 months with 90% mortality at 16 months, significantly reduced from wild-type   (MGI Ref ID J:7454)
    • 64% survival at 24 weeks   (MGI Ref ID J:135036)
  • immune system phenotype
  • abnormal lymph node morphology
    • larger lymph nodes often show extensive hemorrhage and necrosis   (MGI Ref ID J:7454)
    • enlarged lymph nodes
      • by 4 months of age, lymph nodes are increased 10- to 20-fold   (MGI Ref ID J:6638)
      • nodes are 13 times normal size   (MGI Ref ID J:7454)
      • generalized lymphadenopathy   (MGI Ref ID J:135036)
  • decreased interleukin-2 secretion
    • defect in Il2 activity begins during early life and worsens with age; spleen cells show no stimulated Il2 production upon stimulation with concanavalin A   (MGI Ref ID J:6638)
  • enlarged spleen   (MGI Ref ID J:135036)
  • glomerulonephritis
    • immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes   (MGI Ref ID J:7454)
    • interstitial lymphoid infiltration is observed at 6 months; glomerular IgG deposits that are exclusively mesangial are observed   (MGI Ref ID J:135036)
  • increased autoantibody level
    • increase in thymocytotoxic autoantibodies at 6 months is seen   (MGI Ref ID J:7454)
    • mice have elevated levels of anti-chromatin antibodies compared to double mutants   (MGI Ref ID J:135036)
    • increased anti-nuclear antigen antibody level
      • anti-nuclear antibodies are present at 6 months of age   (MGI Ref ID J:6638)
      • mice have significantly increased levels of anti-ssDNA antibodies   (MGI Ref ID J:7454)
      • mice have elevated levels of anti-chromatin (anti-nucleosome) antibodies compared to double mutants   (MGI Ref ID J:135036)
      • increased anti-double stranded DNA antibody level
        • antibodies are increased relative to controls   (MGI Ref ID J:7454)
  • increased double-negative T cell number   (MGI Ref ID J:135036)
  • increased immunoglobulin level
    • IgG and IgM levels are increased in serum at 6 months   (MGI Ref ID J:7454)
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology
    • nephritic changes consist of focal increase in mesangial substance and mild mesangial proliferation   (MGI Ref ID J:7454)
    • expanded mesangial matrix
      • focal increase in mesangial substance   (MGI Ref ID J:7454)
    • glomerulonephritis
      • immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes   (MGI Ref ID J:7454)
      • interstitial lymphoid infiltration is observed at 6 months; glomerular IgG deposits that are exclusively mesangial are observed   (MGI Ref ID J:135036)
    • mesangial cell hyperplasia
      • mild mesangial proliferation   (MGI Ref ID J:7454)
  • hematopoietic system phenotype
  • enlarged spleen   (MGI Ref ID J:135036)
  • increased double-negative T cell number   (MGI Ref ID J:135036)
  • increased immunoglobulin level
    • IgG and IgM levels are increased in serum at 6 months   (MGI Ref ID J:7454)

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

Faslpr/Faslpr

        MRL/Mp-Faslpr
  • mortality/aging
  • premature death
    • mean age of death in females was 17 weeks of age   (MGI Ref ID J:13757)
    • mean age of death in males was 22 weeks of age   (MGI Ref ID J:13757)
    • life span of females is 120+/-4 days   (MGI Ref ID J:28885)
    • life span of males is 154+/-32 days   (MGI Ref ID J:28885)
    • 50% mortality is observed at 5 or 5.5 months for females and males with 90% mortality at 7.3 or 8.6 months in females and males   (MGI Ref ID J:27634)
  • immune system phenotype
  • abnormal B cell morphology
    • frequency of C3d receptor bearing cells declines with age   (MGI Ref ID J:108760)
    • abnormal B cell receptor editing
      • Anti-dsDNA B cells escape receptor editing   (MGI Ref ID J:131138)
    • abnormal marginal zone B cell morphology
      • mice have a larger marginal zone B cell population (10.8% of splenic lymphocytes) compared to BALB/c controls (1.9%)   (MGI Ref ID J:131138)
  • abnormal T cell morphology
    • increase in T-cell frequencies and absolute numbers with advanced disease; however, the number of Ly123+ and Ly23+ T cells is markedly decreased in older mice compared to young mice   (MGI Ref ID J:108760)
    • the proliferating T cell population expresses cell surface markers that are normally expressed by B cells, in addition to normal T cell surface markers   (MGI Ref ID J:6902)
    • mutant Lyt-2- T cells express a cell surface marker that is also expressed on B cells   (MGI Ref ID J:7094)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-   (MGI Ref ID J:8267)
  • abnormal immune system organ morphology   (MGI Ref ID J:28885)
    • abnormal lymph node morphology
      • in mice with lymph node hyperplasia, larger nodes show extensive hemorrhage and cystic necrosis, which results in clinically observed terminal reduction in size   (MGI Ref ID J:27634)
      • abnormal lymph node cell ratio
        • mice show 4- to 6-fold higher frequencies of immunoglobulin-secreting cells (IgSC) compared to normal controls   (MGI Ref ID J:6257)
      • enlarged lymph nodes   (MGI Ref ID J:108760)
        • enlargement started at 8 weeks of age and progressed until lymph node weights were 100 times control lymph node weight by 16 weeks of age   (MGI Ref ID J:13757)
        • node architecture was blurred, with proliferation of lymphocytes with some admixture of plasma cells and histiocytes   (MGI Ref ID J:13757)
        • no evidence of malignancy was present, despite enlargement   (MGI Ref ID J:13757)
        • all mice begin to develop generalized lymph lymphadenopathy when >3 months of age; in about 33%. lymph nodes shrink markedly 7-10 days before death   (MGI Ref ID J:27634)
        • lymph node hyperplasia
          • lymph nodes are up to 100 times normal size   (MGI Ref ID J:27634)
    • abnormal marginal zone B cell morphology
      • mice have a larger marginal zone B cell population (10.8% of splenic lymphocytes) compared to BALB/c controls (1.9%)   (MGI Ref ID J:131138)
    • abnormal thymus cortex morphology   (MGI Ref ID J:28885)
      • atrophic cortex   (MGI Ref ID J:13757)
    • abnormal thymus medulla morphology
      • increase in thymus weight restricted to the medulla   (MGI Ref ID J:28885)
    • enlarged Peyer's patches
      • slight enlargement   (MGI Ref ID J:28885)
    • enlarged spleen
      • spleen is 7-fold larger than controls   (MGI Ref ID J:28885)
    • enlarged thymus
      • slighlty enlarged   (MGI Ref ID J:13757)
      • increased thymus weight
        • doubling of thymus weight   (MGI Ref ID J:28885)
    • thymus atrophy
      • thymic atrophy is observed; severity is most severe in the cortex but usually involves the medulla in most animals   (MGI Ref ID J:27634)
      • initial lesion is loss of cortical thymocytes, with later degeneration (cystic) of thymocytes of medulla   (MGI Ref ID J:27634)
      • in 5-10% of animals, there is medullary or stromal hyperplasia that maintains or increases the size of the thymus   (MGI Ref ID J:27634)
  • abnormal immune system physiology   (MGI Ref ID J:28885)
    • 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 T-helper 2 physiology
        • activity of helper T cells is enhanced in older mice relative to younger animals or normal controls   (MGI Ref ID J:6257)
      • abnormal cytotoxic T cell physiology
        • 4-6 month old mice exhibit significantly depressed cytotoxic T cell response to alloantigens   (MGI Ref ID J:7488)
    • abnormal interleukin level
      • stimulation with concanavalin A does not induce cells to produce Il2   (MGI Ref ID J:8267)
    • abnormal type III hypersensitivity reaction
      • perivascular infiltration of lymphocytes, plasma cells, and histiocytes in lung, kidney, salivary gland and liver   (MGI Ref ID J:28885)
      • perivascular and peribronchial lymphoproliferation observed in lung reslting in patches of atelectasis and exudate containing patches   (MGI Ref ID J:28885)
    • decreased interleukin-2 secretion
      • early in life, mice show reduced Il2 production, that worsens with age, such that almost no Il2 activity is detected in culture supernatants from 2 month old animals; spleen cells show no stimulated Il2 production upon stimulation with concanavalin A   (MGI Ref ID J:6638)
      • mice have severe deficiency in Il-2 production   (MGI Ref ID J:7488)
    • glomerulonephritis
      • immune complex glomerulonephritis   (MGI Ref ID J:13757)
      • glomerular lesions involve proliferation of both endothelial and mesangial cells and basement membrane thickening   (MGI Ref ID J:28885)
      • granular deposits of immunoglobulins present in the capillary walls   (MGI Ref ID J:28885)
      • capsular cell proliferation, tubular damage, and casts were seen in severe lesions   (MGI Ref ID J:28885)
      • mice show a largely subacute proliferative form of disease; lesions involve proliferation of endothelial and mesangial cells   (MGI Ref ID J:27634)
    • increased autoantibody level
      • thymocytoxic autoantibodies are detected with aging   (MGI Ref ID J:28885)
      • increased anti-erythrocyte antigen antibody level
        • levels reach 4 and 11% in males and females   (MGI Ref ID J:27634)
      • increased anti-nuclear antigen antibody level
        • antinuclear antibody titers are detectable at 8 weeks of age and increased rapidly   (MGI Ref ID J:28885)
        • anti-Sm antibodies are detected in males and females but not in controls   (MGI Ref ID J:27634)
        • anti-nuclear antigen antibody (ANA) activity in renal eluate Ig is much higher than activity in serum Ig for anti-ssDNA and anti-dsDNA   (MGI Ref ID J:27634)
        • increased anti-double stranded DNA antibody level
          • 4-month old mice show around 4-fold higher number of spleen cells secreting autoantibodies to dsDNA compared to 8-month old wild-type controls.   (MGI Ref ID J:6257)
          • high levels detected at 4-5 months   (MGI Ref ID J:27634)
          • significant levels of IgM and IgG antibodies that bind dsDNA antibodies are detected in mice 6-8 weeks of age   (MGI Ref ID J:131138)
          • levels of these auto antibodies rise with age   (MGI Ref ID J:131138)
        • increased anti-single stranded DNA antibody level
          • detected at significant levels at 2 months, with very high levels detected at 4-5 months   (MGI Ref ID J:27634)
    • increased immunoglobulin level   (MGI Ref ID J:28885)
      • hypergammaglobulinemia   (MGI Ref ID J:13757)
      • mice show 4- to 6-fold higher frequencies of immunoglobulin-secreting cells in spleens compared to normal controls   (MGI Ref ID J:6257)
      • increased IgA level
        • 2-fold increase   (MGI Ref ID J:28885)
      • increased IgG level
        • at 2-3 months, concentration are up to 5 times control and 8 times control at 5 months   (MGI Ref ID J:27634)
        • increased IgG1 level   (MGI Ref ID J:13757)
          • 10-fold increase   (MGI Ref ID J:28885)
        • increased IgG2a level   (MGI Ref ID J:13757)
          • 10-fold increase   (MGI Ref ID J:28885)
        • increased IgG2b level
          • 2-fold increase   (MGI Ref ID J:28885)
      • increased IgM level
        • 2-fold increase   (MGI Ref ID J:28885)
    • increased susceptibility to autoimmune disorder   (MGI Ref ID J:108760)
    • salivary gland inflammation
      • autoimmune sialodenitis with parenchymal destruction is observed in 4-6 month old mice in submandibular salivary glands of female mice   (MGI Ref ID J:21965)
      • most infiltrating cells are CD4+ and Vbeta8+ with a minority being CD4+ and Vbeta6+   (MGI Ref ID J:21965)
      • lymphocytic infiltration and lymphocytic foci are observed in mice 3.4-3.7 months of age   (MGI Ref ID J:18512)
      • treatment with danazol or Org 4094 sifnificantly lowers number of foci and percentage of lymphocyte infiltration, as well as other immune parameters compared to untreated controls   (MGI Ref ID J:18512)
    • thyroid inflammation
      • animals display thyroid gland infiltration (autoimmune thyroiditis)   (MGI Ref ID J:28171)
    • vascular inflammation
      • arteritis is observed in a number of organs, and is associated with hemorrhage and infarcts in the lymph nodes   (MGI Ref ID J:28885)
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology
    • between 2 and 5 months, granular IgG and C3 deposits increase in capillary wall and mesangium   (MGI Ref ID J:27634)
    • abnormal glomerular capillary morphology
      • granular deposits of immunoglobulins present in the capillary walls   (MGI Ref ID J:28885)
      • abnormal glomerular capillary endothelium morphology
        • proliferation of endothelial cells   (MGI Ref ID J:28885)
    • glomerular crescent
      • capsular cell proliferation is seen in severe glomerular lesions   (MGI Ref ID J:28885)
    • glomerulonephritis
      • immune complex glomerulonephritis   (MGI Ref ID J:13757)
      • glomerular lesions involve proliferation of both endothelial and mesangial cells and basement membrane thickening   (MGI Ref ID J:28885)
      • granular deposits of immunoglobulins present in the capillary walls   (MGI Ref ID J:28885)
      • capsular cell proliferation, tubular damage, and casts were seen in severe lesions   (MGI Ref ID J:28885)
      • mice show a largely subacute proliferative form of disease; lesions involve proliferation of endothelial and mesangial cells   (MGI Ref ID J:27634)
    • mesangial cell hyperplasia
      • proliferation of mesangial cells   (MGI Ref ID J:28885)
  • increased kidney cell proliferation
    • glomerular lesions involve proliferation of endothelial and mesangial cells   (MGI Ref ID J:27634)
  • increased renal glomerulus basement membrane thickness
    • glomerular basement membrane thickening   (MGI Ref ID J:28885)
  • increased urine protein level
    • incomplete penetrance, 50% of females tested have a 9-fold increase over controls   (MGI Ref ID J:28885)
  • renal cast
    • casts were seen in severe glomerular lesions   (MGI Ref ID J:28885)
  • homeostasis/metabolism phenotype
  • abnormal circulating protein level
    • mice have high concentrations of circulating immune complex at 2-3 and 4-5 months   (MGI Ref ID J:27634)
    • high levels of cyroglobulins are found in mice at 5 months   (MGI Ref ID J:27634)
    • increased circulating serum albumin level   (MGI Ref ID J:28885)
    • increased circulating total protein level
      • total serum protein levels are slightly increased   (MGI Ref ID J:28885)
      • 2-fold increase in beta- and 5-fold increase in gamma-globulins   (MGI Ref ID J:28885)
  • abnormal interleukin level
    • stimulation with concanavalin A does not induce cells to produce Il2   (MGI Ref ID J:8267)
  • increased urine protein level
    • incomplete penetrance, 50% of females tested have a 9-fold increase over controls   (MGI Ref ID J:28885)
  • hematopoietic system phenotype
  • abnormal B cell morphology
    • frequency of C3d receptor bearing cells declines with age   (MGI Ref ID J:108760)
    • abnormal B cell receptor editing
      • Anti-dsDNA B cells escape receptor editing   (MGI Ref ID J:131138)
    • abnormal marginal zone B cell morphology
      • mice have a larger marginal zone B cell population (10.8% of splenic lymphocytes) compared to BALB/c controls (1.9%)   (MGI Ref ID J:131138)
  • abnormal T cell morphology
    • increase in T-cell frequencies and absolute numbers with advanced disease; however, the number of Ly123+ and Ly23+ T cells is markedly decreased in older mice compared to young mice   (MGI Ref ID J:108760)
    • the proliferating T cell population expresses cell surface markers that are normally expressed by B cells, in addition to normal T cell surface markers   (MGI Ref ID J:6902)
    • mutant Lyt-2- T cells express a cell surface marker that is also expressed on B cells   (MGI Ref ID J:7094)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-   (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 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 T-helper 2 physiology
      • activity of helper T cells is enhanced in older mice relative to younger animals or normal controls   (MGI Ref ID J:6257)
    • abnormal cytotoxic T cell physiology
      • 4-6 month old mice exhibit significantly depressed cytotoxic T cell response to alloantigens   (MGI Ref ID J:7488)
  • abnormal thymus cortex morphology   (MGI Ref ID J:28885)
    • atrophic cortex   (MGI Ref ID J:13757)
  • abnormal thymus medulla morphology
    • increase in thymus weight restricted to the medulla   (MGI Ref ID J:28885)
  • enlarged spleen
    • spleen is 7-fold larger than controls   (MGI Ref ID J:28885)
  • enlarged thymus
    • slighlty enlarged   (MGI Ref ID J:13757)
    • increased thymus weight
      • doubling of thymus weight   (MGI Ref ID J:28885)
  • increased immunoglobulin level   (MGI Ref ID J:28885)
    • hypergammaglobulinemia   (MGI Ref ID J:13757)
    • mice show 4- to 6-fold higher frequencies of immunoglobulin-secreting cells in spleens compared to normal controls   (MGI Ref ID J:6257)
    • increased IgA level
      • 2-fold increase   (MGI Ref ID J:28885)
    • increased IgG level
      • at 2-3 months, concentration are up to 5 times control and 8 times control at 5 months   (MGI Ref ID J:27634)
      • increased IgG1 level   (MGI Ref ID J:13757)
        • 10-fold increase   (MGI Ref ID J:28885)
      • increased IgG2a level   (MGI Ref ID J:13757)
        • 10-fold increase   (MGI Ref ID J:28885)
      • increased IgG2b level
        • 2-fold increase   (MGI Ref ID J:28885)
    • increased IgM level
      • 2-fold increase   (MGI Ref ID J:28885)
  • thymus atrophy
    • thymic atrophy is observed; severity is most severe in the cortex but usually involves the medulla in most animals   (MGI Ref ID J:27634)
    • initial lesion is loss of cortical thymocytes, with later degeneration (cystic) of thymocytes of medulla   (MGI Ref ID J:27634)
    • in 5-10% of animals, there is medullary or stromal hyperplasia that maintains or increases the size of the thymus   (MGI Ref ID J:27634)
  • cardiovascular system phenotype
  • abnormal cardiovascular system physiology
    • 15-30% of mice suffer old and/or acute myocardial infarction involving either ventricle and judged severe enough to contribute to death   (MGI Ref ID J:27634)
    • vascular inflammation
      • arteritis is observed in a number of organs, and is associated with hemorrhage and infarcts in the lymph nodes   (MGI Ref ID J:28885)
  • abnormal coronary artery morphology   (MGI Ref ID J:27634)
  • abnormal glomerular capillary morphology
    • granular deposits of immunoglobulins present in the capillary walls   (MGI Ref ID J:28885)
    • abnormal glomerular capillary endothelium morphology
      • proliferation of endothelial cells   (MGI Ref ID J:28885)
  • endocrine/exocrine gland phenotype
  • *normal* endocrine/exocrine gland phenotype
    • lymphatic tissues that undergo age-related increase in weight due to lymphocytic accumulation are decreased in weight with cyclophosphamide treatment compared to placebo treated controls   (MGI Ref ID J:18512)
    • abnormal gland morphology
      • dexamethasone treatment increases weight of lacrimal tissue compared to untreated mice; treatment results in a reduction in tear volume   (MGI Ref ID J:18512)
      • abnormal lacrimal gland morphology
        • adult lacrimal glands show infiltration by lymphocytes   (MGI Ref ID J:18512)
        • treatment with steroids alleviates lymphocyte infiltration   (MGI Ref ID J:18512)
      • abnormal submandibular gland morphology
        • treatment with androgens increases gland weight in mutants   (MGI Ref ID J:18512)
        • this treatment significantly decreases lymphocytic infiltration into submandibular glands   (MGI Ref ID J:18512)
      • abnormal thyroid gland morphology
        • inflamed tissue has massive infiltration organized into lymphoid follicle centers and extensive interstitially distributed lymphocytes   (MGI Ref ID J:28171)
        • fibrosis is minimal, with only 1% of tissue displaying fibroblast growth; when detected, fibrosis is adjacent to atrophic follicles   (MGI Ref ID J:28171)
        • functional communication between cells in thyroid cell cultures is dramatically reduced   (MGI Ref ID J:28171)
        • abnormal thymus cortex morphology   (MGI Ref ID J:28885)
          • atrophic cortex   (MGI Ref ID J:13757)
        • abnormal thymus medulla morphology
          • increase in thymus weight restricted to the medulla   (MGI Ref ID J:28885)
        • abnormal thyroid follicle morphology
          • marked decrease in follicle size is noted proceeding from center of lobe toward periphery   (MGI Ref ID J:28171)
        • enlarged thymus
          • slighlty enlarged   (MGI Ref ID J:13757)
          • increased thymus weight
            • doubling of thymus weight   (MGI Ref ID J:28885)
        • thymus atrophy
          • thymic atrophy is observed; severity is most severe in the cortex but usually involves the medulla in most animals   (MGI Ref ID J:27634)
          • initial lesion is loss of cortical thymocytes, with later degeneration (cystic) of thymocytes of medulla   (MGI Ref ID J:27634)
          • in 5-10% of animals, there is medullary or stromal hyperplasia that maintains or increases the size of the thymus   (MGI Ref ID J:27634)
    • salivary gland inflammation
      • autoimmune sialodenitis with parenchymal destruction is observed in 4-6 month old mice in submandibular salivary glands of female mice   (MGI Ref ID J:21965)
      • most infiltrating cells are CD4+ and Vbeta8+ with a minority being CD4+ and Vbeta6+   (MGI Ref ID J:21965)
      • lymphocytic infiltration and lymphocytic foci are observed in mice 3.4-3.7 months of age   (MGI Ref ID J:18512)
      • treatment with danazol or Org 4094 sifnificantly lowers number of foci and percentage of lymphocyte infiltration, as well as other immune parameters compared to untreated controls   (MGI Ref ID J:18512)
    • thyroid inflammation
      • animals display thyroid gland infiltration (autoimmune thyroiditis)   (MGI Ref ID J:28171)
  • skeleton phenotype
  • joint swelling
    • 20-25% of old, diseased mice show joint swelling of the hind feet and lower legs; involving destruction of articular cartilage, proliferation of synovium, pannus formations, and sometimes joint effusions   (MGI Ref ID J:27634)
  • digestive/alimentary phenotype
  • abnormal submandibular gland morphology
    • treatment with androgens increases gland weight in mutants   (MGI Ref ID J:18512)
    • this treatment significantly decreases lymphocytic infiltration into submandibular glands   (MGI Ref ID J:18512)
  • salivary gland inflammation
    • autoimmune sialodenitis with parenchymal destruction is observed in 4-6 month old mice in submandibular salivary glands of female mice   (MGI Ref ID J:21965)
    • most infiltrating cells are CD4+ and Vbeta8+ with a minority being CD4+ and Vbeta6+   (MGI Ref ID J:21965)
    • lymphocytic infiltration and lymphocytic foci are observed in mice 3.4-3.7 months of age   (MGI Ref ID J:18512)
    • treatment with danazol or Org 4094 sifnificantly lowers number of foci and percentage of lymphocyte infiltration, as well as other immune parameters compared to untreated controls   (MGI Ref ID J:18512)
  • vision/eye phenotype
  • abnormal lacrimal gland morphology
    • adult lacrimal glands show infiltration by lymphocytes   (MGI Ref ID J:18512)
    • treatment with steroids alleviates lymphocyte infiltration   (MGI Ref ID J:18512)
  • integument phenotype
  • skin lesions
    • lesions accompanied by hair loss and scab formation were common   (MGI Ref ID J:28885)
    • erythemateous lesions of the ear often become necrotic   (MGI Ref ID J:28885)
  • cellular phenotype
  • increased kidney cell proliferation
    • glomerular lesions involve proliferation of endothelial and mesangial cells   (MGI Ref ID J:27634)

Faslpr/Faslpr

        MRL/MpJ-Faslpr/J
  • mortality/aging
  • premature death
    • 50% mortality is observed at 5 months with 90% mortality at 7.5 months, significantly reduced from wild-type   (MGI Ref ID J:7454)
  • immune system phenotype
  • CNS inflammation
    • at 20 weeks, all mice show mononuclear infiltrates in the choroid plexus; at 10 weeks, all mice display monuclear infiltrates   (MGI Ref ID J:14151)
  • abnormal immunoglobulin level
    • in vitro, splenic B cells produce significantly higher amounts of IgG1 in response to LPS and anti-CD40 plus Il4 stimulation, and higher amounts of IgG2a upon LPS stimulation   (MGI Ref ID J:122315)
    • decreased IgG level
      • production of anti-NP IgG is impaired in spleen cells   (MGI Ref ID J:122315)
    • increased immunoglobulin level
      • IgG and IgM levels are increased in serum at 6 months   (MGI Ref ID J:7454)
      • mice display hypergammaglobulinemia; serum levels are comparable to Fas homozygotes   (MGI Ref ID J:122315)
      • increased IgG level
        • mice exhibit increased serum IgG levels and IgG deposits in the kidney unlike wild-type mice   (MGI Ref ID J:92084)
  • abnormal lymph node morphology
    • larger lymph nodes often show extensive hemorrhage and necrosis   (MGI Ref ID J:7454)
    • enlarged lymph nodes   (MGI Ref ID J:92084)
      • nodes are 62 times normal size   (MGI Ref ID J:7454)
  • conjunctivitis   (MGI Ref ID J:123192)
  • decreased immature B cell number
    • CD19+IgM+ immature B cells are reduced in the spleen   (MGI Ref ID J:122315)
    • decreased transitional stage B cell number
      • numbers of the T1 subset of B cells is reduced   (MGI Ref ID J:122315)
  • decreased mature B cell number
    • CD19+ IgDhigh IgMlow B cells are severely reduced in the spleen   (MGI Ref ID J:122315)
    • decreased marginal zone B cell number
      • numbers of marginal zone (MZ) B cells is reduced   (MGI Ref ID J:122315)
  • decreased spleen germinal center number
    • staining intensity and number of germinal centers (GCs) is reduced 10 days post-challenge with NP-KLH antigen, compared to controls   (MGI Ref ID J:122315)
  • glomerulonephritis   (MGI Ref ID J:92084)
    • severe immune complex glomerulonephritis develops by 6 months   (MGI Ref ID J:7454)
    • mice show deposition of IgG or C3 in kidneys and inflammation, similar to Fas homozygotes   (MGI Ref ID J:122315)
    • kidney lesions have lower scores than those in double mutants at 20 weeks   (MGI Ref ID J:127199)
  • increased autoantibody level
    • at 16 weeks, levels of anti-cardiolipin antibodies are significantly higher than in wild-type controls; levels are significantly higher at 8 weeks   (MGI Ref ID J:14151)
    • mice exhibit increased serum levels of kappa-chain rheumatoid factor compared to in wild-type mice   (MGI Ref ID J:92084)
    • increased anti-nuclear antigen antibody level
      • by 5-6 months of age, Fas-deficient mice have antinuclear antibody (ANA) levels comparable to >50% of C4b-deficient females (on Ighb haplotype homozygous background)   (MGI Ref ID J:111811)
      • at 16 weeks, anti-DNA titers are significantly higher than in wild-type controls   (MGI Ref ID J:14151)
      • mice have significantly increased levels of anti-ssDNA antibodies   (MGI Ref ID J:7454)
      • DNA auto-antibodies are increased compared to in wild-type mice at 12 weeks   (MGI Ref ID J:92084)
      • increased anti-double stranded DNA antibody level   (MGI Ref ID J:92084)
        • antibodies are increased relative to controls and other mutant strains with Faslpr mutations   (MGI Ref ID J:7454)
        • mice produce high titers of IgG1 and IgG2a anti-dsDNA antibodies, comparable to Fas homozygotes   (MGI Ref ID J:122315)
  • increased neutrophil cell number
    • mild to moderated neutrophil accumulation is observed at 20 weeks   (MGI Ref ID J:127199)
  • increased plasma cell number
    • increased B220+IgM+ cells are observed in bone marrow; number of IgG-secreting cells are significantly increased compared to Faslpr homozygotes   (MGI Ref ID J:122315)
  • increased susceptibility to systemic lupus erythematosus
    • mice exhibit increased serum levels of kappa-chain rheumatoid factor and DNA auto-antibodies, lymphadenopathy, glomerulonephritis, renal immunoglobulin deposits, proteinuria, and end organ disease compared to in wild-type mice   (MGI Ref ID J:92084)
  • salivary gland inflammation   (MGI Ref ID J:92084)
  • vasculitis   (MGI Ref ID J:127199)
  • hematopoietic system phenotype
  • abnormal immunoglobulin level
    • in vitro, splenic B cells produce significantly higher amounts of IgG1 in response to LPS and anti-CD40 plus Il4 stimulation, and higher amounts of IgG2a upon LPS stimulation   (MGI Ref ID J:122315)
    • decreased IgG level
      • production of anti-NP IgG is impaired in spleen cells   (MGI Ref ID J:122315)
    • increased immunoglobulin level
      • IgG and IgM levels are increased in serum at 6 months   (MGI Ref ID J:7454)
      • mice display hypergammaglobulinemia; serum levels are comparable to Fas homozygotes   (MGI Ref ID J:122315)
      • increased IgG level
        • mice exhibit increased serum IgG levels and IgG deposits in the kidney unlike wild-type mice   (MGI Ref ID J:92084)
  • decreased immature B cell number
    • CD19+IgM+ immature B cells are reduced in the spleen   (MGI Ref ID J:122315)
    • decreased transitional stage B cell number
      • numbers of the T1 subset of B cells is reduced   (MGI Ref ID J:122315)
  • decreased mature B cell number
    • CD19+ IgDhigh IgMlow B cells are severely reduced in the spleen   (MGI Ref ID J:122315)
    • decreased marginal zone B cell number
      • numbers of marginal zone (MZ) B cells is reduced   (MGI Ref ID J:122315)
  • decreased spleen germinal center number
    • staining intensity and number of germinal centers (GCs) is reduced 10 days post-challenge with NP-KLH antigen, compared to controls   (MGI Ref ID J:122315)
  • increased neutrophil cell number
    • mild to moderated neutrophil accumulation is observed at 20 weeks   (MGI Ref ID J:127199)
  • increased plasma cell number
    • increased B220+IgM+ cells are observed in bone marrow; number of IgG-secreting cells are significantly increased compared to Faslpr homozygotes   (MGI Ref ID J:122315)
  • renal/urinary system phenotype
  • abnormal kidney physiology
    • progressive decline in renal function is observed, during progression to end-stage renal disease   (MGI Ref ID J:127199)
  • abnormal renal glomerulus morphology
    • abnormalities due to severe glomerulonephritis   (MGI Ref ID J:7454)
    • at 20 weeks, lesions show some neutrophil infiltration and hypercellularity   (MGI Ref ID J:127199)
    • tuft necrosis, capsular proliferation and fibrosis are less common and less severe than observed in double mutants   (MGI Ref ID J:127199)
    • cortical renal glomerulopathies
      • glomerulonephritic changes such as hypercellularity, lobularity, dilated capsules and crescent formation or enlarged glomeruli are observed in mice at 3-4 months   (MGI Ref ID J:122315)
      • glomerulonephritis   (MGI Ref ID J:92084)
        • severe immune complex glomerulonephritis develops by 6 months   (MGI Ref ID J:7454)
        • mice show deposition of IgG or C3 in kidneys and inflammation, similar to Fas homozygotes   (MGI Ref ID J:122315)
        • kidney lesions have lower scores than those in double mutants at 20 weeks   (MGI Ref ID J:127199)
    • expanded mesangial matrix
      • mild increase in mesangial matrix is seen at 20 weeks of age   (MGI Ref ID J:127199)
    • glomerular crescent
      • crescent formation is observed in mice at 3-4 months   (MGI Ref ID J:122315)
    • mesangial cell hyperplasia
      • mild increase in mesangial cells is seen at 20 weeks of age   (MGI Ref ID J:127199)
    • renal glomerulus hypertrophy
      • enlarged glomeruli are observed in mice at 3-4 months   (MGI Ref ID J:122315)
  • dilated renal glomerular capsule
    • dilated capsules are observed in mice at 3-4 months   (MGI Ref ID J:122315)
  • increased urine protein level   (MGI Ref ID J:122315)
    • albuminuria
      • mice have excessive urinary albumin compared to wild-type (>10-fold) at 3-4 months   (MGI Ref ID J:122315)
  • podocyte foot process effacement
    • foot processes are only focally effaced   (MGI Ref ID J:127199)
  • behavior/neurological phenotype
  • abnormal spatial learning
    • mice show increased latency to locate hidden platform in water maze testing on days 2-5 of testing at 8 weeks of age; at 16 weeks in spatial bias testing, mutants spend less time and travel reduced distances in quadrant of platform's previous location compared to controls   (MGI Ref ID J:14151)
  • impaired coordination
    • equilibrium is significantly impaired in mice at 18-20 weeks, as measured by performance in rotarod tests   (MGI Ref ID J:14151)
  • vision/eye phenotype
  • *normal* vision/eye phenotype   (MGI Ref ID J:123192)
    • abnormal conjunctival epithelium morphology   (MGI Ref ID J:123192)
    • conjunctivitis   (MGI Ref ID J:123192)
  • cardiovascular system phenotype
  • abnormal myocardium layer morphology
    • myocardium neighboring the heart valves shows mononuclear infiltration of the vessels, but valves are normal   (MGI Ref ID J:14151)
  • vasculitis   (MGI Ref ID J:127199)
  • hearing/vestibular/ear phenotype
  • abnormal stria vascularis morphology
    • slight degenerative changes in the stria vascularis of both the apical and basal turns   (MGI Ref ID J:3638)
    • the basement membrane of the capillaries in the stria vascularis was thickened   (MGI Ref ID J:3638)
    • widened intercellular space in the stria vascularis   (MGI Ref ID J:3638)
    • the basal infolding of strial marginal cells   (MGI Ref ID J:3638)
    • abnormal strial intermediate cell morphology
      • thinned intermediate cell layer   (MGI Ref ID J:3638)
  • increased or absent threshold for auditory brainstem response
    • the ABR threshold f the 20-week-old mutant mice were significantly higher than those of the 4-week-old mutant mice and the 20-week-old wild-type BALB/c mice   (MGI Ref ID J:3638)
  • nervous system phenotype
  • CNS inflammation
    • at 20 weeks, all mice show mononuclear infiltrates in the choroid plexus; at 10 weeks, all mice display monuclear infiltrates   (MGI Ref ID J:14151)
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity
    • 7-8 week old mice show 2-3 fold induction of Dnase1l3 in macrophages and 4-5 fold induction in splenocytes over C57BL/6; levels in other strains like BXSB/MpJ and (NZB x NZW)F1 are similarly elevated compared to B6   (MGI Ref ID J:109815)
    • mice show a dramatic defect (~8-fold decrease) in macrophage-secreted Dnase1l3 barrier to liposomal (BT) activity compared to B6; (NZB x NZW)F1 mice show a similar defect in BT activity   (MGI Ref ID J:109815)
  • increased urine protein level   (MGI Ref ID J:122315)
    • albuminuria
      • mice have excessive urinary albumin compared to wild-type (>10-fold) at 3-4 months   (MGI Ref ID J:122315)
  • pigmentation phenotype
  • abnormal strial intermediate cell morphology
    • thinned intermediate cell layer   (MGI Ref ID J:3638)
  • digestive/alimentary phenotype
  • salivary gland inflammation   (MGI Ref ID J:92084)
  • endocrine/exocrine gland phenotype
  • salivary gland inflammation   (MGI Ref ID J:92084)

Faslpr/Faslpr

        involves: C3H * MRL/Mp
  • immune system phenotype
  • autoimmune response
    • systemic autoimmune disease occurred at 2-3 months of age   (MGI Ref ID J:1060)
    • characterized by elevated serum immune complexes, cryoglobulins, and antinuclear antibodies   (MGI Ref ID J:1060)
    • increased anti-nuclear antigen antibody level
      • beginning at 4 month of age   (MGI Ref ID J:34296)
    • increased susceptibility to systemic lupus erythematosus
      • beginning at 4 month of age   (MGI Ref ID J:34296)
  • increased spleen weight
    • at 2 months of age and on   (MGI Ref ID J:34296)
  • increased susceptibility to type III hypersensitivity reaction
    • beginning at 4 month of age   (MGI Ref ID J:34296)
  • hearing/vestibular/ear phenotype
  • abnormal stria vascularis morphology
    • degeneration of the stria vascularis was seen starting at 2 month and progressed throughout the lifespan   (MGI Ref ID J:1060)
    • early edema of the stria occurred in the apex and progressed basalward   (MGI Ref ID J:1060)
    • by 10 months of age, stria vascularis area was smaller   (MGI Ref ID J:1060)
    • no degeneration of hair cells was seen at any age   (MGI Ref ID J:1060)
    • edematous areas in the stria vascularis primarily in the basal turns due to enlarged extracellular spaces filled with fluid   (MGI Ref ID J:34296)
    • all sensorineural elements, inner and outer hair cells and spiral ganglion neurons appeared normal even in the 8-10 month-old mice with significant threshold shifts   (MGI Ref ID J:34296)
    • abnormal stria vascularis vasculature morphology
      • the stria capillaries often were larger than normal, and the endothelial cells were occasionally swollen or thickened due to hypertrophy and not hyperplasia   (MGI Ref ID J:34296)
  • increased or absent threshold for auditory brainstem response
    • the ABR thresholds of the 10-month-old mutant mice were significantly higher than those of wild-type C3H/HeJ controls   (MGI Ref ID J:1060)
    • the 2- and 4-month-old mutant mice had normal auditory thresholds similar to control   (MGI Ref ID J:34296)
    • after onset of systemic autoimmune disease at 3-4 months of age, threshold at 6 months were significantly elevated at 24 and 32 kHz   (MGI Ref ID J:34296)
    • threshold continued to rise and by 8 months 16 kHz was elevated as well   (MGI Ref ID J:34296)
    • threshold at the low frequencies (4 and 8 kHz) did not change with progression of systemic disease   (MGI Ref ID J:34296)
  • hematopoietic system phenotype
  • increased spleen weight
    • at 2 months of age and on   (MGI Ref ID J:34296)
  • cardiovascular system phenotype
  • abnormal stria vascularis vasculature morphology
    • the stria capillaries often were larger than normal, and the endothelial cells were occasionally swollen or thickened due to hypertrophy and not hyperplasia   (MGI Ref ID J:34296)

Faslpr/Faslpr

        MRL-Faslpr
  • immune system phenotype
  • abnormal T-helper 2 physiology
    • enhanced T-helper cell activity is seen in vitro; removal of T cells from splenic cultures resulted in a significant reduction of the frequency of spontaneous immunoglobulin release in both autoimmune and normal spleen cell populations   (MGI Ref ID J:6257)
    • T cell-enriched populations from older animals provided twice the help offered by T cells of young syngeneic animals or T cells from young and older normal mice of the same H-2 haplotype   (MGI Ref ID J:6257)
  • enlarged lymph nodes
    • mean weight of axillary lymph nodes is 1.3 grams   (MGI Ref ID J:126261)
  • glomerulonephritis
    • lymphocyte infiltration, lobulation, and hyaline deposition noted in kidney   (MGI Ref ID J:126261)
  • increased anti-nuclear antigen antibody level
    • levels are elevated compared to wild-type mice   (MGI Ref ID J:126261)
    • increased anti-double stranded DNA antibody level
      • 30 fold higher than in mice without autoimmune disease   (MGI Ref ID J:126261)
  • increased immunoglobulin level
    • splenic cells in culture show four- to sixfold higher frequencies of spontaneous immunoglobulin release than controls   (MGI Ref ID J:6257)
    • increased IgG level
      • twice wild-type levels   (MGI Ref ID J:126261)
    • increased IgM level
      • about 1.7 fold higher than wild-type levels   (MGI Ref ID J:126261)
  • increased spleen weight
    • mean weight is 0.9 grams   (MGI Ref ID J:126261)
  • vasculitis
    • observed in kidneys with destruction of external elastic lamina common   (MGI Ref ID J:126261)
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level
    • mean levels are 52.4 mg/dl   (MGI Ref ID J:126261)
  • hematopoietic system phenotype
  • abnormal T-helper 2 physiology
    • enhanced T-helper cell activity is seen in vitro; removal of T cells from splenic cultures resulted in a significant reduction of the frequency of spontaneous immunoglobulin release in both autoimmune and normal spleen cell populations   (MGI Ref ID J:6257)
    • T cell-enriched populations from older animals provided twice the help offered by T cells of young syngeneic animals or T cells from young and older normal mice of the same H-2 haplotype   (MGI Ref ID J:6257)
  • increased immunoglobulin level
    • splenic cells in culture show four- to sixfold higher frequencies of spontaneous immunoglobulin release than controls   (MGI Ref ID J:6257)
    • increased IgG level
      • twice wild-type levels   (MGI Ref ID J:126261)
    • increased IgM level
      • about 1.7 fold higher than wild-type levels   (MGI Ref ID J:126261)
  • increased spleen weight
    • mean weight is 0.9 grams   (MGI Ref ID J:126261)
  • cardiovascular system phenotype
  • vasculitis
    • observed in kidneys with destruction of external elastic lamina common   (MGI Ref ID J:126261)
  • renal/urinary system phenotype
  • glomerulonephritis
    • lymphocyte infiltration, lobulation, and hyaline deposition noted in kidney   (MGI Ref ID J:126261)

Faslpr/Faslpr

        MRL.Cg-Irf1tm1Mak Faslpr
  • mortality/aging
  • premature death
    • mice typically die by 26 weeks of age from renal failure; 50% of mice are dead by 22 weeks   (MGI Ref ID J:114771)
  • renal/urinary system phenotype
  • glomerulonephritis
    • at 26 weeks of age, mice show severe glomerulonephritis   (MGI Ref ID J:114771)
    • mice show extensive glomerular deposition/staining of IgG and C3   (MGI Ref ID J:114771)
  • increased urine protein level
    • by 24 weeks of age, 75% of mice have urine protein levels >200 mg/dl   (MGI Ref ID J:114771)
  • kidney failure
    • occurs around 26 weeks, leading to death   (MGI Ref ID J:114771)
  • immune system phenotype
  • glomerulonephritis
    • at 26 weeks of age, mice show severe glomerulonephritis   (MGI Ref ID J:114771)
    • mice show extensive glomerular deposition/staining of IgG and C3   (MGI Ref ID J:114771)
  • increased anti-double stranded DNA antibody level
    • at 26 weeks of age, levels are significantly higher relative to Faslpr, Irf1-null mice   (MGI Ref ID J:114771)
  • homeostasis/metabolism phenotype
  • increased urine protein level
    • by 24 weeks of age, 75% of mice have urine protein levels >200 mg/dl   (MGI Ref ID J:114771)
  • integument phenotype
  • abnormal skin condition
    • mice show characteristic signs of skin disease at 24 weeks of age   (MGI Ref ID J:114771)
  • epidermal necrosis
    • by 24 weeks, ear necrosis is observed in some mice   (MGI Ref ID J:114771)
  • skin lesions   (MGI Ref ID J:114771)

Faslpr/Faslpr

        C3.MRL-Faslpr/J
  • 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
      • 50% mortality is observed at 11.5 months with 90% mortality at 14 months, significantly reduced from wild-type   (MGI Ref ID J:7454)
  • hematopoietic system phenotype
  • abnormal B cell activation
    • after 10 weeks of age, there is a 2-fold increase in frequency of immunoglobulin-containing and secreting cells in the spleen; this does not occur until abnormal T cells (Ly-5(B220+) cells) are found in the spleen   (MGI Ref ID J:7454)
  • abnormal T cell morphology
    • (sIg-, Ly-5(B220+) are present at 4 weeks of age in spleen and by 16-20 weeks, represent 80% of cells   (MGI Ref ID J:7454)
  • decreased eosinophil cell number
    • airway eosinophils are decreased with anti-Il5 teatment compared to contol IgG-teated animals at 96 hours   (MGI Ref ID J:106288)
  • increased immunoglobulin level
    • IgG and IgM levels are increased in serum at 6 months   (MGI Ref ID J:7454)
  • immune system phenotype
  • *normal* immune system phenotype
    • mice show normal spleen and lymph node cell cytotoxic T cell response to alloantigen   (MGI Ref ID J:7454)
    • abnormal B cell activation
      • after 10 weeks of age, there is a 2-fold increase in frequency of immunoglobulin-containing and secreting cells in the spleen; this does not occur until abnormal T cells (Ly-5(B220+) cells) are found in the spleen   (MGI Ref ID J:7454)
    • abnormal T cell morphology
      • (sIg-, Ly-5(B220+) are present at 4 weeks of age in spleen and by 16-20 weeks, represent 80% of cells   (MGI Ref ID J:7454)
    • abnormal lymph node morphology
      • larger lymph nodes often show extensive hemorrhage and necrosis   (MGI Ref ID J:7454)
      • enlarged lymph nodes
        • nodes are 29 times normal size   (MGI Ref ID J:7454)
        • lymph node hyperplasia
          • after 10 weeks of age, there is a 3- to 4-fold increase in numbers of B lymphocytes, and after 6 weeks of age, there is a 4- to 5-fold increase in number of null cells (sIg-, Thy-1-)   (MGI Ref ID J:7454)
    • decreased eosinophil cell number
      • airway eosinophils are decreased with anti-Il5 teatment compared to contol IgG-teated animals at 96 hours   (MGI Ref ID J:106288)
    • decreased interleukin-2 secretion
      • after 6 weeks of age, spleen cells show significant decrease in ability to produce Il-2 induced by concanavalin A treatment   (MGI Ref ID J:7454)
    • glomerulonephritis
      • immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes   (MGI Ref ID J:7454)
    • increased autoantibody level
      • marked increase in thymocytotoxic autoantibodies at 6 months is seen   (MGI Ref ID J:7454)
      • increased anti-nuclear antigen antibody level
        • mice have significantly increased levels of anti-ssDNA antibodies   (MGI Ref ID J:7454)
        • increased anti-double stranded DNA antibody level
          • antibodies are increased relative to controls   (MGI Ref ID J:7454)
    • increased immunoglobulin level
      • IgG and IgM levels are increased in serum at 6 months   (MGI Ref ID J:7454)
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology
    • nephritic changes consist of focal increase in mesangial substance and mild mesangial proliferation   (MGI Ref ID J:7454)
    • expanded mesangial matrix
      • focal increase in mesangial substance   (MGI Ref ID J:7454)
    • glomerulonephritis
      • immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes   (MGI Ref ID J:7454)
    • mesangial cell hyperplasia
      • mild mesangial proliferation   (MGI Ref ID J:7454)
  • cellular phenotype
  • increased apoptosis
    • a trend toward increased apoptosis in airways is observed in anti-Il5 treated mutants after IP-IN OVA challenge   (MGI Ref ID J:106288)
  • respiratory system phenotype
  • abnormal airway responsiveness
    • mice intraperitoneally-injected (IP) with ovalbumin (OVA) and subsequently challenged intranasally (IN) with OVA develop airway hyperresponsiveness (AHR) at 48 hours and is significantly sustained at 96 hours but resolves at 6 days, whereas wild-type mice under same paradigm develop AHR at 48 hours but changes in airway resistance resolve by 96 hours   (MGI Ref ID J:106288)
    • treatment with anti-Il5 at 48 hours post-IP-IN challenge significantly attenuates AHR   (MGI Ref ID J:106288)

Faslpr/Faslpr

        AK.MRL-Faslpr
  • immune system phenotype
  • abnormal lymph node morphology
    • larger lymph nodes often show extensive hemorrhage and necrosis   (MGI Ref ID J:7454)
    • enlarged lymph nodes
      • nodes are 6 times normal size   (MGI Ref ID J:7454)
  • glomerulonephritis
    • immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes   (MGI Ref ID J:7454)
  • increased autoantibody level
    • increase in thymocytotoxic autoantibodies at 6 months is seen   (MGI Ref ID J:7454)
    • increased anti-nuclear antigen antibody level
      • mice have significantly increased levels of anti-ssDNA antibodies   (MGI Ref ID J:7454)
      • increased anti-double stranded DNA antibody level
        • antibodies are increased relative to controls   (MGI Ref ID J:7454)
  • increased immunoglobulin level
    • IgG and IgM levels are modestly increased in serum at 6 months   (MGI Ref ID J:7454)
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology
    • nephritic changes consist of focal increase in mesangial substance and mild mesangial proliferation   (MGI Ref ID J:7454)
    • expanded mesangial matrix
      • focal increase in mesangial substance   (MGI Ref ID J:7454)
    • glomerulonephritis
      • immune complex glomerulonephritis develops by 1 year of age but is much milder than in MRL homozygotes   (MGI Ref ID J:7454)
    • mesangial cell hyperplasia
      • mild mesangial proliferation   (MGI Ref ID J:7454)
  • hematopoietic system phenotype
  • increased immunoglobulin level
    • IgG and IgM levels are modestly increased in serum at 6 months   (MGI Ref ID J:7454)

Faslpr/Faslpr

        C3.MRL-Faslpr
  • 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 proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (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)
  • lacrimal gland inflammation
    • at 2 months, glandular inflammation is neglible; at 5 months, nearly all mice exhibit lacrimal gland inflammation covering a larger area than in mutants at 2 months or controls at 5 months   (MGI Ref ID J:1028)
    • inflammation correlates with age, immune complex level and spleen weight; antinuclear antibody level correlation is greater than probability cutoff; controls do not show correlations with these factors and gland inflammation   (MGI Ref ID J:1028)
    • inflammatory infiltrates consist of mononuclear cells and occurs in a periductal or perivascular pattern   (MGI Ref ID J:1028)
    • scattered lobular atrophy with loss of secretory elements is seen in glands with multifocal infiltrates   (MGI Ref ID J:1028)
  • salivary gland inflammation   (MGI Ref ID J:1028)
  • endocrine/exocrine gland phenotype
  • *normal* endocrine/exocrine gland phenotype
    • submandibular gland inflammation is observed in most mice at 5 months, but differences compared to wild-type are not significant   (MGI Ref ID J:1028)
    • no parotid gland inflammation is observed and only 1 animal showed sublingual gland inflammation at 5 months   (MGI Ref ID J:1028)
    • in inflamed lacrimal glands, lobular boundaries are preserved with preservation of interlobular septae; lobular atrophy occurs with preservation of ductal epithelium; widely dilated ducts indicate that ductal obstruction is not observed   (MGI Ref ID J:1028)
    • lacrimal gland inflammation
      • at 2 months, glandular inflammation is neglible; at 5 months, nearly all mice exhibit lacrimal gland inflammation covering a larger area than in mutants at 2 months or controls at 5 months   (MGI Ref ID J:1028)
      • inflammation correlates with age, immune complex level and spleen weight; antinuclear antibody level correlation is greater than probability cutoff; controls do not show correlations with these factors and gland inflammation   (MGI Ref ID J:1028)
      • inflammatory infiltrates consist of mononuclear cells and occurs in a periductal or perivascular pattern   (MGI Ref ID J:1028)
      • scattered lobular atrophy with loss of secretory elements is seen in glands with multifocal infiltrates   (MGI Ref ID J:1028)
    • salivary gland inflammation   (MGI Ref ID J:1028)
  • 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 proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (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)
  • vision/eye phenotype
  • lacrimal gland inflammation
    • at 2 months, glandular inflammation is neglible; at 5 months, nearly all mice exhibit lacrimal gland inflammation covering a larger area than in mutants at 2 months or controls at 5 months   (MGI Ref ID J:1028)
    • inflammation correlates with age, immune complex level and spleen weight; antinuclear antibody level correlation is greater than probability cutoff; controls do not show correlations with these factors and gland inflammation   (MGI Ref ID J:1028)
    • inflammatory infiltrates consist of mononuclear cells and occurs in a periductal or perivascular pattern   (MGI Ref ID J:1028)
    • scattered lobular atrophy with loss of secretory elements is seen in glands with multifocal infiltrates   (MGI Ref ID J:1028)
  • digestive/alimentary phenotype
  • salivary gland inflammation   (MGI Ref ID J:1028)
  • cellular phenotype
  • decreased apoptosis
    • unlike wild-type vaginal cells, vaginal cells derived from mutant mice do not undergo apoptosis after treatment with agonistic anti-mouse Fas antibody or mouse recombinant TNF antibody   (MGI Ref ID J:114219)
    • 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   (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   (MGI Ref ID J:124252)
  • 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   (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   (MGI Ref ID J:124252)
  • reproductive system phenotype
  • abnormal vagina weight
    • at 2 days after estrogen deprivation induced by gonadectomy, mutant females show no vaginal regression (measured by a decrease in vaginal organ weight), indicating no Fas-mediated vaginal cell death, in contrast to wild-type females that show >50% decrease in vaginal organ weight   (MGI Ref ID J:114219)

Faslpr/Faslpr

        MRL/MpJ-Faslpr
  • mortality/aging
  • premature death
    • 50% mortality by 20 weeks; <40% survival beyond 40 weeks   (MGI Ref ID J:137066)
    • animals start to die at 4.5 months, with >50% mortality observed at 7 months   (MGI Ref ID J:125114)
  • hematopoietic system phenotype
  • abnormal leukocyte adhesion
    • significantly enhanced at 12 and 16 weeks   (MGI Ref ID J:126009)
  • abnormal leukocyte morphology
    • 46% of venules display leukocytes adjacent to endothelium, compared to only 145 in controls; in mutants and controls, 60-70% of these cells are mononuclear   (MGI Ref ID J:126009)
    • decreased B cell number   (MGI Ref ID J:137066)
    • decreased CD4-positive, alpha beta T cell number
      • reduced compared to wild-type MRL animals   (MGI Ref ID J:137066)
    • decreased CD8-positive, alpha-beta T cell number
      • reduced compared to wild-type MRL animals   (MGI Ref ID J:137066)
    • decreased activated T cell number   (MGI Ref ID J:137066)
    • increased double-negative T cell number
      • significantly increased relative to controls   (MGI Ref ID J:137066)
  • abnormal leukocyte tethering or rolling
    • rolling is dramatically reduced, but not eliminated, in mutants compared to controls   (MGI Ref ID J:126009)
    • in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated   (MGI Ref ID J:126009)
  • enlarged spleen
  • increased immunoglobulin level
    • mice develop hypergammaglobulinemia   (MGI Ref ID J:125114)
  • immune system phenotype
  • abnormal leukocyte adhesion
    • significantly enhanced at 12 and 16 weeks   (MGI Ref ID J:126009)
  • abnormal leukocyte morphology
    • 46% of venules display leukocytes adjacent to endothelium, compared to only 145 in controls; in mutants and controls, 60-70% of these cells are mononuclear   (MGI Ref ID J:126009)
    • decreased B cell number   (MGI Ref ID J:137066)
    • decreased CD4-positive, alpha beta T cell number
      • reduced compared to wild-type MRL animals   (MGI Ref ID J:137066)
    • decreased CD8-positive, alpha-beta T cell number
      • reduced compared to wild-type MRL animals   (MGI Ref ID J:137066)
    • decreased activated T cell number   (MGI Ref ID J:137066)
    • increased double-negative T cell number
      • significantly increased relative to controls   (MGI Ref ID J:137066)
  • abnormal leukocyte tethering or rolling
    • rolling is dramatically reduced, but not eliminated, in mutants compared to controls   (MGI Ref ID J:126009)
    • in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated   (MGI Ref ID J:126009)
  • autoimmune response
    • mice develop anti-nuclear antibodies (ie. anti-dsDNA, anti-ssDNA, etc)   (MGI Ref ID J:125114)
    • increased autoantibody level
      • IgG3 anti-IgG2a rheumatoid factor (RF) levels are much higher than wild-type controls   (MGI Ref ID J:137066)
      • increased anti-nuclear antigen antibody level
        • levels of anti-dsDNA and anti-chromatin autoantibodies are elevated compared to wild-type   (MGI Ref ID J:137066)
  • enlarged lymph nodes
  • enlarged spleen
  • glomerulonephritis   (MGI Ref ID J:132514)
    • mice show deposition of IgG or C3 in kidneys and inflammation   (MGI Ref ID J:125114)
  • increased immunoglobulin level
    • mice develop hypergammaglobulinemia   (MGI Ref ID J:125114)
  • vascular inflammation
    • mice develop systemic necrotizing arteritis of small- and medium-sized arteries; frequently observed in kidneys   (MGI Ref ID J:137066)
  • cardiovascular system phenotype
  • vascular inflammation
    • mice develop systemic necrotizing arteritis of small- and medium-sized arteries; frequently observed in kidneys   (MGI Ref ID J:137066)
  • renal/urinary system phenotype
  • glomerulonephritis   (MGI Ref ID J:132514)
    • mice show deposition of IgG or C3 in kidneys and inflammation   (MGI Ref ID J:125114)
  • cellular phenotype
  • abnormal leukocyte adhesion
    • significantly enhanced at 12 and 16 weeks   (MGI Ref ID J:126009)
  • abnormal leukocyte tethering or rolling
    • rolling is dramatically reduced, but not eliminated, in mutants compared to controls   (MGI Ref ID J:126009)
    • in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated   (MGI Ref ID J:126009)

Faslpr/Faslpr

        involves: MRL/Mp
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • mice exhibit increased Pseudomonas aerugiosa exotoxin-induced mortality compared with similarly treated wild-type mice   (MGI Ref ID J:50903)
  • immune system phenotype
  • decreased macrophage apoptosis
    • macrophages exhibit 60% less cholesterol-induced apoptosis compared with similarly treated wild-type cells   (MGI Ref ID J:154647)
  • increased susceptibility to bacterial infection
    • mice exhibit increased Pseudomonas aerugiosa exotoxin-induced mortality compared with similarly treated wild-type mice   (MGI Ref ID J:50903)
  • cellular phenotype
  • decreased macrophage apoptosis
    • macrophages exhibit 60% less cholesterol-induced apoptosis compared with similarly treated wild-type cells   (MGI Ref ID J:154647)
  • hematopoietic system phenotype
  • decreased macrophage apoptosis
    • macrophages exhibit 60% less cholesterol-induced apoptosis compared with similarly treated wild-type cells   (MGI Ref ID J:154647)

Faslpr/Faslpr

        involves: C57BL/6 * MRL/Mp
  • immune system phenotype
  • enlarged spleen
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgA level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG1 level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG2a level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG2b level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG3 level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgM level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased anti-double stranded DNA antibody level
    • at day 275   (MGI Ref ID J:73396)
  • increased anti-single stranded DNA antibody level
    • at day 275   (MGI Ref ID J:73396)
  • lymph node hyperplasia
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • hematopoietic system phenotype
  • enlarged spleen
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgA level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG1 level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG2a level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG2b level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgG3 level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)
  • increased IgM level
    • at day 175 and 275 compared with wild-type mice   (MGI Ref ID J:73396)

Faslpr/Faslpr

        involves: 129P2/OlaHsd * MRL
  • mortality/aging
  • premature death
    • about 10% of mice are moribund by 16 weeks of age   (MGI Ref ID J:26250)
  • immune system phenotype
  • enlarged lymph nodes
    • develop massive lymphadenopathy due to alpha beta DN T cell accumulation   (MGI Ref ID J:26250)
  • increased double-negative T cell number
    • develop massive lymphadenopathy due to alpha beta DN T cell accumulation   (MGI Ref ID J:26250)
  • increased gamma-delta T cell number   (MGI Ref ID J:26250)
  • kidney inflammation
    • periglomerular infiltration   (MGI Ref ID J:45448)
    • glomerulonephritis
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level
    • significantly elevated   (MGI Ref ID J:45448)
  • increased urine protein level
    • compared to age-matched B10.A mice   (MGI Ref ID J:45448)
  • renal/urinary system phenotype
  • abnormal kidney morphology   (MGI Ref ID J:45448)
    • abnormal renal glomerulus morphology
      • glomerular hypercellularity   (MGI Ref ID J:45448)
      • glomerulonephritis
  • increased urine protein level
    • compared to age-matched B10.A mice   (MGI Ref ID J:45448)
  • kidney inflammation
    • periglomerular infiltration   (MGI Ref ID J:45448)
  • hematopoietic system phenotype
  • increased double-negative T cell number
    • develop massive lymphadenopathy due to alpha beta DN T cell accumulation   (MGI Ref ID J:26250)
  • increased gamma-delta T cell number   (MGI Ref ID J:26250)
View Research Applications

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

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
      lupus erythematosus

Faslpr related

Apoptosis Research
Death Receptors

Cancer Research
Genes Regulating Growth and Proliferation

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
      lupus erythematosus
      lupus erythematosus: rheumatoid arthritis
Inflammation
      rheumatoid arthritis

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Faslpr
Allele Name lymphoproliferation
Allele Type Spontaneous
Common Name(s) Fas-; Fas-def; MRL/lpr; Tnfrf6lpr; Tnfrsf6lpr; Tnfrsf6lpr; lpr;
Strain of OriginMRL/Mp
Gene Symbol and Name Fas, Fas (TNF receptor superfamily member 6)
Chromosome 19
Gene Common Name(s) AI196731; ALPS1A; APO-1; APT1; CD95; FAS1; FASTM; TNF receptor superfamily member 6; TNFR6; TNFRSF6; Tnfrsf6; expressed sequence AI196731; lpr; lymphoproliferation;
General Note Faslpr, lymphoproliferation, recessive. This mutation was found during inbreeding of a strain MRL/Mp derived from crosses among strains LG, AKR, C3H, and C57BL/6. The resemblance has led to extensive use of Faslpr mice in attemptsto determine the etiology of SLE and to evaluate therapies. However, the human APT1 gene (OMIM 134637) encodes the FAS antigen; Tnfrsf6 is not the homolog of the human (SLE) gene.The Cd72c haplotype is a modifier of Faslpr-induced autoimmune disease. J:204782
Molecular Note Southern blotting experiments indicated that the mutation is a genomic rearrangement within the gene, probably within intron 2. [MGI Ref ID J:1181] [MGI Ref ID J:14206] [MGI Ref ID J:14503] [MGI Ref ID J:15429] [MGI Ref ID J:4166] [MGI Ref ID J:4342]

Genotyping

Genotyping Information

Genotyping Protocols

Faslpr MCA, Melt Curve Analysis
NntC57BL/6J,

Separated MCA


Faslpr, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Faslpr related

Adachi K; Tsutsui H; Kashiwamura S; Seki E; Nakano H; Takeuchi O; Takeda K; Okumura K; Van Kaer L; Okamura H; Akira S; Nakanishi K. 2001. Plasmodium berghei infection in mice induces liver injury by an IL-12- and toll-like receptor/myeloid differentiation factor 88-dependent mechanism. J Immunol 167(10):5928-34. [PubMed: 11698470]  [MGI Ref ID J:118004]

Adachi M; Watanabe-Fukunaga R; Nagata S. 1993. Aberrant transcription caused by the insertion of an early transposable element in an intron of the Fas antigen gene of lpr mice. Proc Natl Acad Sci U S A 90(5):1756-60. [PubMed: 7680478]  [MGI Ref ID J:4342]

Affourtit C; Jastroch M; Brand MD. 2011. Uncoupling protein-2 attenuates glucose-stimulated insulin secretion in INS-1E insulinoma cells by lowering mitochondrial reactive oxygen species. Free Radic Biol Med 50(5):609-16. [PubMed: 21172424]  [MGI Ref ID J:168471]

Ahuja A; Teichmann LL; Wang H; Dunn R; Kehry MR; Shlomchik MJ. 2011. An acquired defect in IgG-dependent phagocytosis explains the impairment in antibody-mediated cellular depletion in Lupus. J Immunol 187(7):3888-94. [PubMed: 21873531]  [MGI Ref ID J:179332]

Aicher WK; Fujihashi K; Yamamoto M; Kiyono H; Pitts AM; McGhee JR. 1992. Effects of the lpr/lpr mutation on T and B cell populations in the lamina propria of the small intestine, a mucosal effector site. Int Immunol 4(9):959-68. [PubMed: 1390438]  [MGI Ref ID J:3154]

Ait-Azzouzene D; Kono DH; Gonzalez-Quintial R; McHeyzer-Williams LJ; Lim M; Wickramarachchi D; Gerdes T; Gavin AL; Skog P; McHeyzer-Williams MG; Nemazee D; Theofilopoulos AN. 2010. Deletion of IgG-switched autoreactive B cells and defects in Fas(lpr) lupus mice. J Immunol 185(2):1015-27. [PubMed: 20554953]  [MGI Ref ID J:161936]

Akashi T; Nagafuchi S; Anzai K; Kitamura D; Wang J; Taniuchi I; Niho Y; Watanabe T. 1998. Proliferation of CD3+ B220- single-positive normal T cells was suppressed in B-cell-deficient lpr mice. Immunology 93(2):238-48. [PubMed: 9616374]  [MGI Ref ID J:45808]

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]

Al Gadban MM; German J; Truman JP; Soodavar F; Riemer EC; Twal WO; Smith KJ; Heller D; Hofbauer AF; Oates JC; Hammad SM. 2012. Lack of nitric oxide synthases increases lipoprotein immune complex deposition in the aorta and elevates plasma sphingolipid levels in lupus. Cell Immunol 276(1-2):42-51. [PubMed: 22560558]  [MGI Ref ID J:188295]

Al-Shami A; Crisostomo J; Wilkins C; Xu N; Humphries J; Chang WC; Anderson SJ; Oravecz T. 2013. Integrin-alpha FG-GAP repeat-containing protein 2 is critical for normal B cell differentiation and controls disease development in a lupus model. J Immunol 191(7):3789-98. [PubMed: 23997217]  [MGI Ref ID J:205951]

Alarcon-Riquelme ME; Fernandez C. 1995. CDR3 regions in the preimmune VH B cell repertoire of lpr mice. Clin Exp Immunol 101(1):73-7. [PubMed: 7621595]  [MGI Ref ID J:26829]

Alarcon-Riquelme ME; Fernandez C. 1995. Expression of the B cell repertoire in lpr mice; abnormal expansion of a few VHJ558 germ-line genes. Clin Exp Immunol 99(2):262-8. [PubMed: 7851020]  [MGI Ref ID J:22861]

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 JJ; Jacob A; Bao L; Macdonald RL; Quigg RJ. 2005. Complement-dependent apoptosis and inflammatory gene changes in murine lupus cerebritis. J Immunol 175(12):8312-9. [PubMed: 16339572]  [MGI Ref ID J:122254]

Alexander JJ; Jacob A; Vezina P; Sekine H; Gilkeson GS; Quigg RJ. 2007. Absence of functional alternative complement pathway alleviates lupus cerebritis. Eur J Immunol 37(6):1691-701. [PubMed: 17523212]  [MGI Ref ID J:123511]

Alexander JJ; Zwingmann C; Jacob A; Quigg R. 2007. Alteration in kidney glucose and amino acids are implicated in renal pathology in MRL/lpr mice. Biochim Biophys Acta 1772(10):1143-9. [PubMed: 17942282]  [MGI Ref ID J:130687]

Alexander JJ; Zwingmann C; Quigg R. 2005. MRL/lpr mice have alterations in brain metabolism as shown with [1H-13C] NMR spectroscopy. Neurochem Int 47(1-2):143-51. [PubMed: 15893408]  [MGI Ref ID J:129820]

Ali M; Weinreich M; Balcaitis S; Cooper CJ; Fink PJ. 2003. Differential regulation of peripheral CD4+ T cell tolerance induced by deletion and TCR revision. J Immunol 171(11):6290-6. [PubMed: 14634147]  [MGI Ref ID J:132828]

Allam R; Pawar RD; Kulkarni OP; Hornung V; Hartmann G; Segerer S; Akira S; Endres S; Anders HJ. 2008. Viral 5'-triphosphate RNA and non-CpG DNA aggravate autoimmunity and lupus nephritis via distinct TLR-independent immune responses. Eur J Immunol 38(12):3487-3498. [PubMed: 19009528]  [MGI Ref ID J:141388]

Allison J; Thomas HE; Catterall T; Kay TW; Strasser A. 2005. Transgenic expression of dominant-negative Fas-associated death domain protein in beta cells protects against Fas ligand-induced apoptosis and reduces spontaneous diabetes in nonobese diabetic mice. J Immunol 175(1):293-301. [PubMed: 15972661]  [MGI Ref ID J:100606]

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]

Altman A. 1994. Abnormal antigen receptor-initiated signal transduction in lpr T lymphocytes. Semin Immunol 6(1):9-17. [PubMed: 7513195]  [MGI Ref ID J:19053]

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Zhang B; Hirahashi J; Cullere X; Mayadas TN. 2003. Elucidation of molecular events leading to neutrophil apoptosis following phagocytosis: cross-talk between caspase 8, reactive oxygen species, and MAPK/ERK activation. J Biol Chem 278(31):28443-54. [PubMed: 12736263]  [MGI Ref ID J:120441]

Zhang B; Kracker S; Yasuda T; Casola S; Vanneman M; Homig-Holzel C; Wang Z; Derudder E; Li S; Chakraborty T; Cotter SE; Koyama S; Currie T; Freeman GJ; Kutok JL; Rodig SJ; Dranoff G; Rajewsky K. 2012. Immune Surveillance and Therapy of Lymphomas Driven by Epstein-Barr Virus Protein LMP1 in a Mouse Model. Cell 148(4):739-51. [PubMed: 22341446]  [MGI Ref ID J:181546]

Zhang B; Maris CH; Foell J; Whitmire J; Niu L; Song J; Kwon BS; Vella AT; Ahmed R; Jacob J; Mittler RS. 2007. Immune suppression or enhancement by CD137 T cell costimulation during acute viral infection is time dependent. J Clin Invest 117(10):3029-41. [PubMed: 17853940]  [MGI Ref ID J:127406]

Zhang MC; Furukawa H; Tokunaka K; Saiga K; Date F; Owada Y; Nose M; Ono M. 2008. Mast cell hyperplasia in the skin of Dsg4-deficient hypotrichosis mice, which are long-living mutants of lupus-prone mice. Immunogenetics 60(10):599-607. [PubMed: 18677469]  [MGI Ref ID J:140028]

Zhang X; Shan P; Alam J; Davis RJ; Flavell RA; Lee PJ. 2003. Carbon monoxide modulates Fas/Fas ligand, caspases, and Bcl-2 family proteins via the p38alpha mitogen-activated protein kinase pathway during ischemia-reperfusion lung injury. J Biol Chem 278(24):22061-70. [PubMed: 12690100]  [MGI Ref ID J:211469]

Zhang XK; Gallant S; Molano I; Moussa OM; Ruiz P; Spyropoulos DD; Watson DK; Gilkeson G. 2004. Decreased expression of the Ets family transcription factor Fli-1 markedly prolongs survival and significantly reduces renal disease in MRL/lpr mice. J Immunol 173(10):6481-9. [PubMed: 15528390]  [MGI Ref ID J:94287]

Zhang Z; Kyttaris VC; Tsokos GC. 2009. The role of IL-23/IL-17 axis in lupus nephritis. J Immunol 183(5):3160-9. [PubMed: 19657089]  [MGI Ref ID J:151862]

Zhao Z; Deocharan B; Scherer PE; Ozelius LJ; Putterman C. 2006. Differential binding of cross-reactive anti-DNA antibodies to mesangial cells: the role of alpha-actinin. J Immunol 176(12):7704-14. [PubMed: 16751418]  [MGI Ref ID J:132348]

Zheng L; Sharma R; Gaskin F; Fu SM; Ju ST. 2007. A novel role of IL-2 in organ-specific autoimmune inflammation beyond regulatory T cell checkpoint: both IL-2 knockout and Fas mutation prolong lifespan of Scurfy mice but by different mechanisms. J Immunol 179(12):8035-41. [PubMed: 18056343]  [MGI Ref ID J:155041]

Zhou T; Bluethmann H; Eldridge J; Berry K; Mountz JD. 1993. Origin of CD4-CD8-B220+ T cells in MRL-lpr/lpr mice. Clues from a T cell receptor beta transgenic mouse. J Immunol 150(8 Pt 1):3651-67. [PubMed: 7682246]  [MGI Ref ID J:4525]

Zhou T; Edwards CK 3rd; Yang P; Wang Z; Bluethmann H; Mountz JD. 1996. Greatly accelerated lymphadenopathy and autoimmune disease in lpr mice lacking tumor necrosis factor receptor I. J Immunol 156(8):2661-5. [PubMed: 8609380]  [MGI Ref ID J:32463]

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Zielinski CE; Jacob SN; Bouzahzah F; Ehrlich BE; Craft J. 2005. Naive CD4+ T cells from lupus-prone Fas-intact MRL mice display TCR-mediated hyperproliferation due to intrinsic threshold defects in activation. J Immunol 174(8):5100-9. [PubMed: 15814741]  [MGI Ref ID J:98149]

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Zoukhri D; Kublin CL. 2001. Impaired neurotransmitter release from lacrimal and salivary gland nerves of a murine model of Sjogren's syndrome. Invest Ophthalmol Vis Sci 42(5):925-32. [PubMed: 11274068]  [MGI Ref ID J:68663]

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 Ref ID J:121029]

Zuo J; Ge H; Zhu G; Matthias P; Sun J. 2007. OBF-1 is essential for the generation of antibody-secreting cells and the development of autoimmunity in MRL-lpr mice. J Autoimmun 29(2-3):87-96. [PubMed: 17574818]  [MGI Ref ID J:125114]

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de Lema GP; Maier H; Franz TJ; Escribese M; Chilla S; Segerer S; Camarasa N; Schmid H; Banas B; Kalaydjiev S; Busch DH; Pfeffer K; Mampaso F; Schlondorff D; Luckow B. 2005. Chemokine receptor Ccr2 deficiency reduces renal disease and prolongs survival in MRL/lpr lupus-prone mice. J Am Soc Nephrol 16(12):3592-601. [PubMed: 16267157]  [MGI Ref ID J:113343]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX1

Colony Maintenance

Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $95.50Female or MaleHomozygous for Faslpr  
4 weeks $95.50Female or MaleHomozygous for Faslpr  
5 weeks $95.50Female or MaleHomozygous for Faslpr  
6 weeks $98.95Female or MaleHomozygous for Faslpr  
7 weeks $102.40Female or MaleHomozygous for Faslpr  
8 weeks $105.85Female or MaleHomozygous for Faslpr  
Price per Pair (US dollars $)Pair Genotype
$197.90Homozygous for Faslpr x Homozygous for Faslpr  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $124.20Female or MaleHomozygous for Faslpr  
4 weeks $124.20Female or MaleHomozygous for Faslpr  
5 weeks $124.20Female or MaleHomozygous for Faslpr  
6 weeks $128.70Female or MaleHomozygous for Faslpr  
7 weeks $133.20Female or MaleHomozygous for Faslpr  
8 weeks $137.70Female or MaleHomozygous for Faslpr  
Price per Pair (US dollars $)Pair Genotype
$257.30Homozygous for Faslpr x Homozygous for Faslpr  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.

Cryopreserved

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

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.


See Terms of Use tab for General Terms and Conditions


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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

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.

No Liability

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.


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