cellular phenotype

• increased splenocyte proliferation
  • splenocytes from BCG infected mice exhibit increased proliferation in response to Con A
  (MGI Ref ID J:66802)

immune system phenotype

• abnormal macrophage physiology
  • macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge
  (MGI Ref ID J:66802)
  • macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge
  (MGI Ref ID J:66802)

• abnormal MHC II cell surface expression on macrophages
  • macrophages from BCG infected mice exhibit reduced class II expression
  (MGI Ref ID J:66802)

• abnormal NK cell physiology
  • Normal - however, the recruitment of T cells by IL12 is not impaired
  (MGI Ref ID J:115033)
  • recruitment of NK cells to the liver by recombinant murine IL12 is impaired
  (MGI Ref ID J:115033)
  • significantly lower resting splenic NK cell activity
  (MGI Ref ID J:66802)

• abnormal type IV hypersensitivity reaction
  • exposure to UVA and UVB fails to significantly reduce the UVB induced suppression of the type IV hypersensitivity reaction
  (MGI Ref ID J:55740)
  • Normal - however, the type IV hypersensitivity reaction in the absence of UV exposure is similar to controls
  (MGI Ref ID J:55740)

• decreased length of allograft survival
  • reduced surival of cardiac grafts relative to controls
  (MGI Ref ID J:44346)

• decreased susceptibility to parasitic infection
  • Normal - however, IFNG-competent alpha+CD4+ T cells promote experimental cerebral malaria
  (MGI Ref ID J:189794)
  • mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice
  (MGI Ref ID J:189794)

• decreased susceptibility to parasitic infection induced morbidity/mortality
  • mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice
  (MGI Ref ID J:189794)

• increased splenocyte proliferation
  • splenocytes from BCG infected mice exhibit increased proliferation in response to Con A
  (MGI Ref ID J:66802)

• increased susceptibility to bacterial infection
  • increased mortality following a sublethal dose of Mycobacterium bovis (BCG )
  (MGI Ref ID J:66802)

craniofacial phenotype

• alveolar process atrophy
  • modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks
  (MGI Ref ID J:147935)

integument phenotype

• abnormal skin physiology
  • following exposure to UVA and UVB mice fail to develop significant erythema unlike wild-type controls
  (MGI Ref ID J:55740)
  • Normal - however, the increase in skin fold thickness in response to UVB or UVA and UVB exposure is not significantly different from controls
  (MGI Ref ID J:55740)

growth/size/body region phenotype

• alveolar process atrophy
  • modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks
  (MGI Ref ID J:147935)

mammalian phenotype

• immune system phenotype
  • Normal - mice are able to clear infections of Pneumocystis carinii, similar to controls
  (MGI Ref ID J:119206)

mortality/aging

• decreased susceptibility to parasitic infection induced morbidity/mortality
  • mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice
  (MGI Ref ID J:189794)

neoplasm

• decreased tumor incidence
  • tumor-bearing mice treated with Th-17-polarized cells from Tg(Tcra,Tcrb)9Rest cells show increased tumor rejection compared to controls
  (MGI Ref ID J:138466)

• increased metastatic potential
  • following treatment with alphaGalCer, mice fail to exhibit a reduction in the number of B16F10 tumors metastasizing to the lungs unlike similarly treated wild-type mice
  (MGI Ref ID J:152785)

skeleton phenotype

• alveolar process atrophy
  • modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks
  (MGI Ref ID J:147935)

hematopoietic system phenotype

• abnormal macrophage physiology
  • macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge
  (MGI Ref ID J:66802)
  • macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge
  (MGI Ref ID J:66802)

• abnormal MHC II cell surface expression on macrophages
  • macrophages from BCG infected mice exhibit reduced class II expression
  (MGI Ref ID J:66802)

• abnormal NK cell physiology
  • Normal - however, the recruitment of T cells by IL12 is not impaired
  (MGI Ref ID J:115033)
  • recruitment of NK cells to the liver by recombinant murine IL12 is impaired
  (MGI Ref ID J:115033)
  • significantly lower resting splenic NK cell activity
  (MGI Ref ID J:66802)

• increased splenocyte proliferation
  • splenocytes from BCG infected mice exhibit increased proliferation in response to Con A
  (MGI Ref ID J:66802)

cardiovascular system phenotype

• corneal vascularization
  • corneal injection of a plasmid encoding short hairpin RNA targeting the C terminus of the secreted form of Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice
  (MGI Ref ID J:114973)

hematopoietic system phenotype

• abnormal immunoglobulin level
  • in mice with acute or chronic HSV-1 infection the ratio of IgG2a to IgG1 is dramatically reduced compared to BALB/c wild-type mice
  (MGI Ref ID J:29170)

• impaired natural killer cell mediated cytotoxicity
  • activated splenic and liver NK cells are less efficient in their killing of 4T1 or Renca tumor target cells
  (MGI Ref ID J:73948)

• increased IgG1 level
  • following infection with type A influenza
  (MGI Ref ID J:110721)

mortality/aging

• increased susceptibility to bacterial infection induced morbidity/mortality
  • mean survival time following infecting with virulent Mycobacterium tuberculosis is 15 days compared to over 60 days for wild-type controls
  (MGI Ref ID J:110856)
  • treatment with exogenous IFNG improves survival
  (MGI Ref ID J:110856)

• increased susceptibility to Herpesvirales infection induced morbidity/mortality
  • more than 70% of mice infected on the cornea with herpes simplex virus type 1 (HSV-1) at a dose of 10⁵ TCID50 (50% tissue culture infective dose) infectious particles die
  (MGI Ref ID J:29170)

• increased susceptibility to viral infection induced morbidity/mortality
  • more than 70% of mice infected on the cornea with herpes simplex virus type 1 (HSV-1) at a dose of 10⁵ TCID50 (50% tissue culture infective dose) infectious particles die
  (MGI Ref ID J:29170)

vision/eye phenotype

• corneal vascularization
  • corneal injection of a plasmid encoding short hairpin RNA targeting the C terminus of the secreted form of Flt1 (pshRNA-sflt1) induces corneal vascularization within 3 days of injection in wild-type and mutant mice
  (MGI Ref ID J:114973)

homeostasis/metabolism phenotype

• abnormal cytokine level
  • T cells from mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide show more IL-17a expressing cells and greater IL-17a production after MOG restimulation than controls; IL-4 is not detectable in these cells
  (MGI Ref ID J:112600)

immune system phenotype

• abnormal cytokine level
  • T cells from mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide show more IL-17a expressing cells and greater IL-17a production after MOG restimulation than controls; IL-4 is not detectable in these cells
  (MGI Ref ID J:112600)

• abnormal immunoglobulin level
  • in mice with acute or chronic HSV-1 infection the ratio of IgG2a to IgG1 is dramatically reduced compared to BALB/c wild-type mice
  (MGI Ref ID J:29170)

• abnormal response to infection
  • display an increased IgG1 antibody response to type A influenza infection
  (MGI Ref ID J:110721)
  • the magnitude of the delayed type hypersensitive response in mice after HSV-1 infection is reduced compared to BALB/c wild-type controls
  (MGI Ref ID J:29170)

• decreased susceptibility to type IV hypersensitivity reaction
  • the magnitude of the delayed type hypersensitive response in mice after HSV-1 infection is reduced compared to BALB/c wild-type controls
  (MGI Ref ID J:29170)

• impaired natural killer cell mediated cytotoxicity
  • activated splenic and liver NK cells are less efficient in their killing of 4T1 or Renca tumor target cells
  (MGI Ref ID J:73948)

• increased IgG1 level
  • following infection with type A influenza
  (MGI Ref ID J:110721)

• increased interleukin-17 secretion
  • following culturing of IL-17 producing T cells in vitro, IL-17 production is twice as high as in similarly treated wild-type cells
  (MGI Ref ID J:132905)

• increased susceptibility to bacterial infection
  • at 14 days after infection with virulent Mycobacterium tuberculosis, 10- 100 fold more viable bacteria are found in the organs compared to organs of wild-type controls
  (MGI Ref ID J:110856)
  • at 14 days after infection with virulent Mycobacterium tuberculosis, about 90% of the granulomas in the liver and 20% of the granulomas in the spleen are necrotic
  (MGI Ref ID J:110856)
  • treatment with exogenous IFNG decreases the bacterial load
  (MGI Ref ID J:110856)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • mean survival time following infecting with virulent Mycobacterium tuberculosis is 15 days compared to over 60 days for wild-type controls
  (MGI Ref ID J:110856)
  • treatment with exogenous IFNG improves survival
  (MGI Ref ID J:110856)

• increased susceptibility to Herpesvirales infection
  • at 5 - 8 days post infection mice develop more severe conjunctivitis, periocular skin lesions, corneal opacity, and anterior chamber exudate following infection with HSV-1 relative to wld-type BALB/c controls infected with a higher dose of virus
  (MGI Ref ID J:29170)
  • infectious virus is detected up to 10 days post infection with HSV-1 in mutants compared to up to 4 or days post infection in wild-type BAL/c mice or littermate controls, respectively
  (MGI Ref ID J:29170)

• increased susceptibility to Herpesvirales infection induced morbidity/mortality
  • more than 70% of mice infected on the cornea with herpes simplex virus type 1 (HSV-1) at a dose of 10⁵ TCID50 (50% tissue culture infective dose) infectious particles die
  (MGI Ref ID J:29170)

• increased susceptibility to viral infection
  • at 5 - 8 days post infection mice develop more severe conjunctivitis, periocular skin lesions, corneal opacity, and anterior chamber exudate following infection with HSV-1 relative to wld-type BALB/c controls infected with a higher dose of virus
  (MGI Ref ID J:29170)
  • infectious virus is detected up to 10 days post infection with HSV-1 in mutants compared to up to 4 or days post infection in wild-type BAL/c mice or littermate controls, respectively
  (MGI Ref ID J:29170)

• increased susceptibility to viral infection induced morbidity/mortality
  • more than 70% of mice infected on the cornea with herpes simplex virus type 1 (HSV-1) at a dose of 10⁵ TCID50 (50% tissue culture infective dose) infectious particles die
  (MGI Ref ID J:29170)

behavior/neurological phenotype

• abnormal response to new environment
  • Background Sensitivity - increase in the number of defecations in a novel environment compared to wild-type controls in mice on a C57BL/6 background but not in mice on a BALB/c background
  (MGI Ref ID J:54250)
  • initial locomotor activity is decreased; however, overall distance traveled is not different from controls
  (MGI Ref ID J:54250)
  • the number of rearings is decreased in a novel environment
  (MGI Ref ID J:54250)

• decreased vertical activity
  • in a novel environment
  (MGI Ref ID J:54250)

• increased fear-related response
  • Background Sensitivity - increase in the number of defecations following a sound stimulus suggesting an enhancement of fear related responses in mice on a C57BL/6 background but not in mice on a BALB/c background
  (MGI Ref ID J:54250)
  • make fewer entries and spend less time in the open arms of an elevated maze relative to wild-type controls
  (MGI Ref ID J:54250)
  • prolonged freeze time and longer time to return to normal open field activity patterns following a startle stimulus relative to wild-type controls
  (MGI Ref ID J:54250)

digestive/alimentary phenotype

• stomach inflammation
  • 5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice
  (MGI Ref ID J:120556)

hematopoietic system phenotype

• abnormal dendritic cell chemotaxis
  • enhancement in LPS induced dendritic cell migration to the spleen
  (MGI Ref ID J:134949)
  • enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro
  (MGI Ref ID J:134949)

• abnormal immunoglobulin level
  • IgG responses are restricted to IgG1 and IgG2b
  (MGI Ref ID J:45665)

• abnormal macrophage chemotaxis
  • 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
  (MGI Ref ID J:136628)

• abnormal spleen morphology
  (MGI Ref ID J:47459)

• abnormal spleen red pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
  (MGI Ref ID J:47459)

• abnormal spleen white pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
  (MGI Ref ID J:47459)

• enlarged spleen
  • develop splenomegaly after infection with BCG
  (MGI Ref ID J:47459)

• extramedullary hematopoiesis
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased granulocyte number
  • in the blood, bone marrow and spleen following infection with BCG
  (MGI Ref ID J:47459)

• increased leukocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased monocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased NK T cell number
  • unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers
  (MGI Ref ID J:122801)

• pale spleen
  • spleens become paler as BCG infection proceeds
  (MGI Ref ID J:47459)

homeostasis/metabolism phenotype

• abnormal circulating cytokine level
  • increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
  (MGI Ref ID J:47459)

• abnormal nitric oxide homeostasis
  • unlike in wild-type mice, treatment with LPS and DGalN fails to increase nitric oxide levels
  (MGI Ref ID J:122801)

• abnormal response to injury
  • 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
  (MGI Ref ID J:136628)
  • decrease in the number and area of regenerating muscle fibers 5 and 10 days after muscle injury
  (MGI Ref ID J:136628)
  • fibrotic lesions are sometimes seen after injury
  (MGI Ref ID J:136628)

• abnormal urine homeostasis
  • 1 day after induction of accelerated antiglomerular basement membrane nephritis no increase in total urinary nitrate or nitrate levels is detected unlike in similarly treated wild-type controls
  (MGI Ref ID J:118730)

• albuminuria
  • increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis
  (MGI Ref ID J:118730)

• decreased susceptibility to injury
  • following a 48 h exposure to hyperoxia (98-99% oxygen) neutrophil migration into the lung air space and the increase in pulmonary alveolar permeability are decreased indicating a decrease susceptibility to the early phase of hyperoxia induced lung injury
  (MGI Ref ID J:108148)
  • Normal - however, after 84 h of exposure to hyperoxia these measures are not different from similarly exposed to wild-type controls
  (MGI Ref ID J:108148)

• increased circulating interleukin-6 level
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased sensitivity to xenobiotic induced morbidity/mortality
  • increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls
  (MGI Ref ID J:91927)

immune system phenotype

• abnormal circulating cytokine level
  • increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
  (MGI Ref ID J:47459)

• abnormal cytokine secretion
  (MGI Ref ID J:120556)

• abnormal dendritic cell antigen presentation
  • dendritic cells show a greater ability to stimulate T cell proliferation in vitro
  (MGI Ref ID J:134949)

• abnormal dendritic cell chemotaxis
  • enhancement in LPS induced dendritic cell migration to the spleen
  (MGI Ref ID J:134949)
  • enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro
  (MGI Ref ID J:134949)

• abnormal dendritic cell physiology
  • increase in IL12 and decrease in IL10 secretion following LPS stimulation
  (MGI Ref ID J:134949)

• abnormal humoral immune response
  • however, following oral OVA exposure OVA antibody levels in response to subcutaneous OVA challenge are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels
  (MGI Ref ID J:45665)
  • the magnitude of the OVA specific antibody response to subcutaneous OVA challenge is reduced
  (MGI Ref ID J:45665)

• abnormal immune tolerance
  • oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent subcutaneous exposure to the same antigen
  (MGI Ref ID J:45665)

• abnormal immunoglobulin level
  • IgG responses are restricted to IgG1 and IgG2b
  (MGI Ref ID J:45665)

• abnormal Langerhans cell physiology
  • enhancement in hapten induced Langerhan cell migration to the draining lymph nodes
  (MGI Ref ID J:134949)

• abnormal macrophage chemotaxis
  • 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
  (MGI Ref ID J:136628)

• abnormal spleen morphology
  (MGI Ref ID J:47459)

• abnormal spleen red pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
  (MGI Ref ID J:47459)

• abnormal spleen white pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
  (MGI Ref ID J:47459)

• abnormal type IV hypersensitivity reaction
  • in OVA fed mice only a modest decrease in the delayed type hypersensitivity response to injected OVA is seen in contrast this reaction is strongly decreased in similarly treated wild-type controls
  (MGI Ref ID J:45665)

• decreased interferon-gamma secretion
  • splenocytes fail to produce IFN-gamma in response to H. pylori antigen stimulation
  (MGI Ref ID J:120556)

• decreased interleukin-10 secretion
  • by bone marrow dendritic cells following LPS stimulation
  (MGI Ref ID J:134949)
  • splenocytes from Helicobacter pylori infected mice produce 4-fold less IL-10 when cultured in the presence of H. pylori antigen
  (MGI Ref ID J:120556)

• decreased length of allograft survival
  • decrease in survival times of heart transplants from CBA mice after a 30 day course of anti-CD4 and anti-CD8 mAb
  (MGI Ref ID J:44346)
  • only 10% of heart grafts survive more than 100 days compared to 36% of grafts in wild-type mice
  (MGI Ref ID J:44346)

• enlarged mesenteric lymph nodes
  • in C. parvum infected mice
  (MGI Ref ID J:50832)

• enlarged spleen
  • develop splenomegaly after infection with BCG
  (MGI Ref ID J:47459)

• glomerulonephritis
  • increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes
  (MGI Ref ID J:118730)

• increased circulating interleukin-6 level
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased granulocyte number
  • in the blood, bone marrow and spleen following infection with BCG
  (MGI Ref ID J:47459)

• increased interleukin-12 secretion
  • by bone marrow dendritic cells following LPS stimulation
  (MGI Ref ID J:134949)

• increased interleukin-4 secretion
  • splenocytes from Helicobacter pylori infected mice produce significantly more IL-4 than splenocytes from wild-type controls when cultured in the presence of H. pylori antigen
  (MGI Ref ID J:120556)

• increased leukocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased monocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased NK T cell number
  • unlike in wild-type mice, treatment with LPS and DGalN fails to decrease NK T cell numbers
  (MGI Ref ID J:122801)

• increased susceptibility to bacterial infection
  • following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen
  (MGI Ref ID J:47459)
  • following infection with BCG mice display an increased bacterial load throughout the infect in contrast to wild-type mice where bacterial numbers peak at 17 days post infection and decline thereafter
  (MGI Ref ID J:47459)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
  (MGI Ref ID J:47459)

• increased susceptibility to parasitic infection
  • Background Sensitivity - d in about 50% of mice gallbladders are enlarged
  (MGI Ref ID J:50832)
  • Background Sensitivity - in C. parvum infected mice on a C57BL/6 background, but not on a BALB/c background, the gastrointestinal tract is heavily colonized with parasites, the small intestines are distended and filled with gelatinous fluid, mesenteric lymph nodes are enlarged and in about 50% of mice gallbladders are enlarged
  (MGI Ref ID J:50832)
  • Background Sensitivity - mice on a C57BL/6 background lose weight and develop soft gelatinous stools over the course of a C. parvum infection while mice on a BALB/c background do not
  (MGI Ref ID J:50832)

• increased susceptibility to parasitic infection induced morbidity/mortality
  • most mice die by 9 days after infection with 1x10⁶ Cryptosporidium parvum oocysts
  (MGI Ref ID J:50832)

• increased susceptibility to type IV hypersensitivity reaction
  • display a more severe delayed type hypersensitivity reaction in response to sheep IgG
  (MGI Ref ID J:118730)

• pale spleen
  • spleens become paler as BCG infection proceeds
  (MGI Ref ID J:47459)

• stomach inflammation
  • 5 weeks after Helicobacter pylori infection, mice have a significantly decreased gastritis inflammation score compared to infected wild-type mice
  (MGI Ref ID J:120556)

cellular phenotype

• abnormal dendritic cell chemotaxis
  • enhancement in LPS induced dendritic cell migration to the spleen
  (MGI Ref ID J:134949)
  • enhancement in the ability of dendritic cells to transmigrate across a membrane in response to RANTES in vitro
  (MGI Ref ID J:134949)

• abnormal macrophage chemotaxis
  • 5 days after muscle injury fewer macrophages are present at the injury site compared to similarly treated wild-type mice
  (MGI Ref ID J:136628)

• abnormal redox activity
  • unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase the production of reactive oxygen species in hepatocytes
  (MGI Ref ID J:122801)

mammalian phenotype

• immune system phenotype
  • Normal - do not exhibit defects on either IgE isotype switch or IgE production
  (MGI Ref ID J:114783)

mortality/aging

• increased sensitivity to xenobiotic induced morbidity/mortality
  • increase in mortality following a single dose of N-methyl-N-nitrosourea (MNU) compared to similarly treated wild-type controls
  (MGI Ref ID J:91927)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
  (MGI Ref ID J:47459)

• increased susceptibility to parasitic infection induced morbidity/mortality
  • most mice die by 9 days after infection with 1x10⁶ Cryptosporidium parvum oocysts
  (MGI Ref ID J:50832)

muscle phenotype

• impaired skeletal muscle regeneration
  • decrease in the number and area of regenerating fibers 5 and 10 days after injury
  (MGI Ref ID J:136628)
  • fibrotic lesions are sometimes seen after injury
  (MGI Ref ID J:136628)
  • Normal - however, prior to injury no difference in muscle fiber morphology are detected
  (MGI Ref ID J:136628)

• skeletal muscle fibrosis
  • fibrotic lesions are sometimes seen after injury
  (MGI Ref ID J:136628)

renal/urinary system phenotype

• abnormal urine homeostasis
  • 1 day after induction of accelerated antiglomerular basement membrane nephritis no increase in total urinary nitrate or nitrate levels is detected unlike in similarly treated wild-type controls
  (MGI Ref ID J:118730)

• albuminuria
  • increase in albuminuria on days 2, 3,and 4 following induction of accelerated antiglomerular basement membrane nephritis
  (MGI Ref ID J:118730)

• glomerulonephritis
  • increased susceptibility to induced accelerated antiglomerular basement membrane nephritis as determined by increased albuminuria and more severe pathological changes
  (MGI Ref ID J:118730)

endocrine/exocrine gland phenotype

• increased T cell derived lymphoma incidence
  • in a few mice
  (MGI Ref ID J:77491)

immune system phenotype

• abnormal B cell physiology
  • immature B cells fail to be excluded from the lymph nodes
  (MGI Ref ID J:112084)

• abnormal cytokine secretion
  • after infection with Leishmania major the number of lymphocytes producing IL4 increases unlike in control mice where the number of lymphocytes producing IFNG increases
  (MGI Ref ID J:18801)
  • following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
  (MGI Ref ID J:110826)

• abnormal immunoglobulin level
  (MGI Ref ID J:18801)

• abnormal lymph node cell ratio
  • significant increase in the numbers of immature B cells in the lymph nodes
  (MGI Ref ID J:112084)

• abnormal response to infection
  • after infection with Leishmania major levels of IgG1 and IgE are increased while levels of IgG2a and IgG3 remain low
  (MGI Ref ID J:18801)
  • after infection with Leishmania major mice display minimal Th1 type responses and increased Th2 type responses
  (MGI Ref ID J:18801)
  • following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
  (MGI Ref ID J:110826)

• abnormal response to transplant
  • after immunosuppressive treatment (anti-CD4 and anti-CD8 mAbs) allografts (BALB/c, H2-Ab1^bm12 continue to display myocardial rejection at week 12 but do not display graft arterial disease, in contrast wild-type mice at week 12 display low levels of rejection but develop coronary arteriopathy
  (MGI Ref ID J:42090)
  • s of rejection but develop coronary arteriopathy
  (MGI Ref ID J:42090)

• decreased IgG2a level
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• decreased IgG3 level
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased CD8-positive, alpha-beta T cell number
  • increase in the number of CD8+ cells in the white matter tracts of JHMV infected mice compared to similarly infected wild-type controls at 7 and 14 days post infection
  (MGI Ref ID J:112048)

• increased IgE level
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased IgG1 level
  • 5-fold increase in the serum levels of JHMV specific IgG1 at 14 days post infection compared to infected wild-type controls
  (MGI Ref ID J:112048)
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased interleukin-10 secretion
  • cervical lymph node cells from JHMV infected mice (7 days post infection) secrete more IL10 in response to JHMV antigen compared to cells from similarly infected wild-type mice
  (MGI Ref ID J:112048)

• increased interleukin-2 secretion
  • cervical lymph node cells from JHMV infected mice secrete more IL2 in response to JHMV antigen compared to cells from similarly infected wild-type mice
  (MGI Ref ID J:112048)

• increased interleukin-5 secretion
  • cervical lymph node cells from JHMV infected mice (7 days post infection) secrete more IL5 in response to JHMV antigen compared to cells from similarly infected wild-type mice
  (MGI Ref ID J:112048)

• increased susceptibility to Coronaviridae infection
  • at 14 days post infection with JHMV a 10 fold increase in the number of viral antigen positive cells is detected in the brain with most of the infected cells being oligodendrocytes
  (MGI Ref ID J:112048)
  • following infection with the JHM strain of mouse hepatitis virus (JHMV) mice display a slower clinical recovery and higher viral titers in the central nervous system compared to wild-type controls
  (MGI Ref ID J:112048)
  • Normal - however, no differences are found in JHMV specific cytotoxic T lymphocyte activity
  (MGI Ref ID J:112048)

• increased susceptibility to Coronaviridae infection induced morbidity/mortality
  • higher mortality is seen following infection with JHMV compared to wild-type controls
  (MGI Ref ID J:112048)

• increased susceptibility to parasitic infection
  • develop progressive infection characterized by large lesions at the site of inoculation and sudden death 5 to 7 weeks after infection with Leishmania major
  (MGI Ref ID J:18801)
  • numbers of parasites present in the footpads are substantially increased compared to wild-type and heterozygous controls
  (MGI Ref ID J:18801)

• increased susceptibility to parasitic infection induced morbidity/mortality
  • die earlier after inoculation with Toxoplasma gondii (strain ME49) compared to wild-type controls
  (MGI Ref ID J:110826)
  • sudden death occurs 5 to 7 weeks after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased susceptibility to viral infection
  • at 14 days post infection with JHMV a 10 fold increase in the number of viral antigen positive cells is detected in the brain with most of the infected cells being oligodendrocytes
  (MGI Ref ID J:112048)
  • following infection with the JHM strain of mouse hepatitis virus (JHMV) mice display a slower clinical recovery and higher viral titers in the central nervous system compared to wild-type controls
  (MGI Ref ID J:112048)
  • Normal - however, no differences are found in JHMV specific cytotoxic T lymphocyte activity
  (MGI Ref ID J:112048)

• increased susceptibility to viral infection induced morbidity/mortality
  • higher mortality is seen following infection with JHMV compared to wild-type controls
  (MGI Ref ID J:112048)

hematopoietic system phenotype

• abnormal B cell physiology
  • immature B cells fail to be excluded from the lymph nodes
  (MGI Ref ID J:112084)

• abnormal immunoglobulin level
  (MGI Ref ID J:18801)

• decreased IgG2a level
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• decreased IgG3 level
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased CD8-positive, alpha-beta T cell number
  • increase in the number of CD8+ cells in the white matter tracts of JHMV infected mice compared to similarly infected wild-type controls at 7 and 14 days post infection
  (MGI Ref ID J:112048)

• increased IgE level
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased IgG1 level
  • 5-fold increase in the serum levels of JHMV specific IgG1 at 14 days post infection compared to infected wild-type controls
  (MGI Ref ID J:112048)
  • after infection with Leishmania major
  (MGI Ref ID J:18801)

mortality/aging

• increased susceptibility to Coronaviridae infection induced morbidity/mortality
  • higher mortality is seen following infection with JHMV compared to wild-type controls
  (MGI Ref ID J:112048)

• increased susceptibility to parasitic infection induced morbidity/mortality
  • die earlier after inoculation with Toxoplasma gondii (strain ME49) compared to wild-type controls
  (MGI Ref ID J:110826)
  • sudden death occurs 5 to 7 weeks after infection with Leishmania major
  (MGI Ref ID J:18801)

• increased susceptibility to viral infection induced morbidity/mortality
  • higher mortality is seen following infection with JHMV compared to wild-type controls
  (MGI Ref ID J:112048)

• premature death
  • Background Sensitivity - in mice on a C57BL/6 background compared to mice on a BALB/c background
  (MGI Ref ID J:77491)

neoplasm

• decreased tumor latency
  • Background Sensitivity - in mice on a C57BL/6 background compared to mice on a BALB/c background
  (MGI Ref ID J:77491)

• increased lymphoma incidence
  • Background Sensitivity - 50% of mice on a congenic C57BL/5 background develop disseminated lymphomas compared to 0% of mice on a congenic BALB/c background
  (MGI Ref ID J:77491)
  • most lymphomas are diffuse large cell lymphomas
  (MGI Ref ID J:77491)

• increased sarcoma incidence
  • in a few mice
  (MGI Ref ID J:77491)

• increased T cell derived lymphoma incidence
  • in a few mice
  (MGI Ref ID J:77491)

immune system phenotype

• increased susceptibility to bacterial infection
  • by 4 weeks after aerosol infection with the virulent Erdam strain of Mycobacterium tuberculosis mice display multifocal necrotic areas contain high numbers of bacteria in the spleen, liver, lungs and kidneys
  (MGI Ref ID J:15723)
  • following infection with a sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice develop widespread infection with high numbers of bacteria in multiple tissues and obvious bacteremia
  (MGI Ref ID J:15723)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • after infection with a normally sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice become severely ill and need to be euthanized
  (MGI Ref ID J:15723)

mortality/aging

• increased susceptibility to bacterial infection induced morbidity/mortality
  • after infection with a normally sublethal dose of the virulent Erdam strain of Mycobacterium tuberculosis mice become severely ill and need to be euthanized
  (MGI Ref ID J:15723)

hematopoietic system phenotype

• abnormal immunoglobulin level
  • IgG responses are restricted to IgG1 and IgG2b
  (MGI Ref ID J:45665)

immune system phenotype

• abnormal cytokine secretion
  • following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
  (MGI Ref ID J:110826)

• abnormal humoral immune response
  • Normal - following oral OVA exposure OVA antibody levels are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels
  (MGI Ref ID J:45665)
  • however, following oral OVA exposure OVA antibody levels are essentially unchanged unlike in wild-type controls where oral exposure reduces antibody levels
  (MGI Ref ID J:45665)
  • the magnitude of the OVA specific antibody is reduced
  (MGI Ref ID J:45665)

• abnormal immune tolerance
  • oral exposure to antigen (OVA) fails to reduce the responsiveness of mice to subsequent exposure to the same antigen
  (MGI Ref ID J:45665)

• abnormal immunoglobulin level
  • IgG responses are restricted to IgG1 and IgG2b
  (MGI Ref ID J:45665)

• abnormal response to infection
  • following infection with T. gondii (irradiate RH strain) splenocytes show enhanced Th2 cytokine production compared to similar cultures from wild-type mice
  (MGI Ref ID J:110826)

• increased interleukin-5 secretion
  • following infection with T. gondii (irradiate RH strain) splenocytes produce more IL-5 compared to similar cultures from wild-type mice
  (MGI Ref ID J:110826)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • Normal - following vaccination mice are able to develop resistance to L. monocytogenes infection
  (MGI Ref ID J:83180)
  • Normal - however the LD50 for a mutant strain of L. monocytogenes (DP-L1942) is similar in homozygous mice and controls
  (MGI Ref ID J:83180)
  • the LD50 for Listeria monocytogenes infection is 10 CFU compared to greater than 10⁴ CFU for wild-type and heterozygous controls
  (MGI Ref ID J:83180)

• increased susceptibility to experimental autoimmune encephalomyelitis
  • immunized mice display meningeal and perivascular inflammatory infiltrates in the spinal cord and brain similar to those seen in susceptible strains like SJL/J
  (MGI Ref ID J:34161)
  • incidence rate (17 of 24 compared to 1 of 16 in controls) and severity are increased compared to contols immunization results in about a 30% mortality rate
  (MGI Ref ID J:34161)

• increased susceptibility to parasitic infection
  • 5 days after inoculation with T. gondii (strain ME49) peritoneal exudates contain a more pronounced increase in the numbers of granulocytes, eosinophils, and mast cells compared to similarly infected wild-type controls
  (MGI Ref ID J:110826)
  • dramatic increase in the number of infected cells expansion of the tissues infected following inoculation with Toxoplasma gondii (strain ME49)
  (MGI Ref ID J:110826)
  • Normal - IL-2 production in response to infection is similar to controls
  (MGI Ref ID J:110826)

• increased susceptibility to parasitic infection induced morbidity/mortality
  • die within 9 days of inoculation with T. gondii (strain ME49) unlike controls which survive more than 30 days
  (MGI Ref ID J:110826)
  • highly susceptible to the normally avirulent T. gondii isolate, ts4
  (MGI Ref ID J:110826)

mammalian phenotype

• neoplasm
  • Background Sensitivity - unlike mice on a congenic C57BL/6 background, mice on a BALB/c background do not develop disseminated lymphomas
  (MGI Ref ID J:77491)

mortality/aging

• increased susceptibility to bacterial infection induced morbidity/mortality
  • Normal - following vaccination mice are able to develop resistance to L. monocytogenes infection
  (MGI Ref ID J:83180)
  • Normal - however the LD50 for a mutant strain of L. monocytogenes (DP-L1942) is similar in homozygous mice and controls
  (MGI Ref ID J:83180)
  • the LD50 for Listeria monocytogenes infection is 10 CFU compared to greater than 10⁴ CFU for wild-type and heterozygous controls
  (MGI Ref ID J:83180)

• increased susceptibility to parasitic infection induced morbidity/mortality
  • die within 9 days of inoculation with T. gondii (strain ME49) unlike controls which survive more than 30 days
  (MGI Ref ID J:110826)
  • highly susceptible to the normally avirulent T. gondii isolate, ts4
  (MGI Ref ID J:110826)

neoplasm

• increased lung adenocarcinoma incidence
  • all are well differentiated papillary adenocarcinomas
  (MGI Ref ID J:77491)
  • in a few mice, with a very late onset
  (MGI Ref ID J:77491)

• increased tumor latency
  • Background Sensitivity - in mice on a BALB/c background compared to mice on a C57BL/6 background
  (MGI Ref ID J:77491)

respiratory system phenotype

• increased lung adenocarcinoma incidence
  • all are well differentiated papillary adenocarcinomas
  (MGI Ref ID J:77491)
  • in a few mice, with a very late onset
  (MGI Ref ID J:77491)

mammalian phenotype

• immune system phenotype
  • Background Sensitivity - at generation N4 no difference is seen in the time course of diabetes development in females unlike in mice at generation N7
  (MGI Ref ID J:33427)

hematopoietic system phenotype

• decreased IgE level
  • ovalbumin challenge fails to significantly potentiate ovalbumin specific IgE levels, unlike in wild-type controls
  (MGI Ref ID J:114213)

immune system phenotype

• altered susceptibility to infection
  • mice are able to clear infectious Murine gammaherpesvirus 68 (MHV-68) from their lungs but with a slight delay relative wild-type mice
  (MGI Ref ID J:39478)
  • Normal - no differences are detected in the frequency of latently infected cells, the generation of cytotoxic T cells, the infection induced cytokine profile, or the recruitment or proliferation of cells into inflammatory sites
  (MGI Ref ID J:39478)

• decreased IgE level
  • ovalbumin challenge fails to significantly potentiate ovalbumin specific IgE levels, unlike in wild-type controls
  (MGI Ref ID J:114213)

• decreased inflammatory response
  • the eosinophilic response in ovalbumin challenged mice is reduced compared to wild-type controls
  (MGI Ref ID J:114213)

mammalian phenotype

• immune system phenotype
  • Normal - no difference in survival, tissue damage or spread of infection following infection with the opportunistic fungal pathogen Candida albicans is detected relative to wild-type controls
  (MGI Ref ID J:39881)

respiratory system phenotype

• decreased airway responsiveness
  • ovalbumin challenge fails to induce airway hyperresponsiveness unlike in wild-type mice
  (MGI Ref ID J:114213)

• increased airway responsiveness
  • in saline challenged mice relative to wild-type controls
  (MGI Ref ID J:114213)

behavior/neurological phenotype

• abnormal response to new environment
  • the number of rearings is decreased in a novel environment
  (MGI Ref ID J:54250)
  • Background Sensitivity - unlike mice on a C57BL/6 background, no increase in the number of defecations in a novel environment or following a sound stimulus is seen in mice on a BALB/c background, compared to wild-type controls
  (MGI Ref ID J:54250)

• decreased vertical activity
  • in a novel environment
  (MGI Ref ID J:54250)

• increased fear-related response
  • Background Sensitivity - no increase in the number of defecations following a sound stimulus is seen in mice on a BALB/c background unlike mice on a C57BL/6 background
  (MGI Ref ID J:54250)
  • prolonged freeze time following a startle stimulus relative to wild-type controls
  (MGI Ref ID J:54250)

hematopoietic system phenotype

• abnormal cytotoxic T cell physiology
  • C26 cells induce slightly reduced CTL activity compared to the response in similarly treat wild-type mice
  (MGI Ref ID J:115144)

• abnormal macrophage physiology
  • exposure to rIL12 fails to prime macrophages against subsequent LPS exposure
  (MGI Ref ID J:115144)

• abnormal NK cell physiology
  • decrease in the cytotoxicity of NK cells from mice primed with rIL12
  (MGI Ref ID J:115144)

• abnormal spleen morphology
  (MGI Ref ID J:115144)

• abnormal spleen red pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
  (MGI Ref ID J:47459)

• abnormal spleen white pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
  (MGI Ref ID J:47459)

• abnormal uterine NK cell morphology
  • the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
  (MGI Ref ID J:56503)

• abnormal uterine NK cell physiology
  • decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation
  (MGI Ref ID J:56503)
  • uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
  (MGI Ref ID J:56503)

• enlarged spleen
  • develop splenomegaly after infection with BCG
  (MGI Ref ID J:47459)

• extramedullary hematopoiesis
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased granulocyte number
  • in the blood, bone marrow and spleen following infection with BCG
  (MGI Ref ID J:47459)

• increased leukocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased monocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased uterine NK cell number
  • after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
  (MGI Ref ID J:56503)

• pale spleen
  • spleens become paler as BCG infection proceeds
  (MGI Ref ID J:47459)

homeostasis/metabolism phenotype

• abnormal circulating cytokine level
  • increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
  (MGI Ref ID J:47459)

• increased circulating interleukin-6 level
  • following infection with BCG
  (MGI Ref ID J:47459)

immune system phenotype

• abnormal adaptive immunity
  (MGI Ref ID J:115144)

• abnormal circulating cytokine level
  • increase in circulating levels of CSF3 after infection with BCG especially in moribund mice
  (MGI Ref ID J:47459)

• abnormal cytokine secretion
  • lymphocytes form C25/Il12 cell primed mice produce about 3 fold higher levels of CSF2
  (MGI Ref ID J:115144)

• abnormal cytotoxic T cell physiology
  • C26 cells induce slightly reduced CTL activity compared to the response in similarly treat wild-type mice
  (MGI Ref ID J:115144)

• abnormal inflammatory response
  • in C26/Il12 tumors CD4+ T cells are more numerous relative to CD8+ T cells, in tumors in wild-type mice CD8+ T cells are more numerous
  (MGI Ref ID J:115144)

• abnormal macrophage physiology
  • exposure to rIL12 fails to prime macrophages against subsequent LPS exposure
  (MGI Ref ID J:115144)

• abnormal NK cell physiology
  • decrease in the cytotoxicity of NK cells from mice primed with rIL12
  (MGI Ref ID J:115144)

• abnormal spleen morphology
  (MGI Ref ID J:115144)

• abnormal spleen red pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the red pulp is replaced with extramedullary hematopoietic tissue
  (MGI Ref ID J:47459)

• abnormal spleen white pulp morphology
  • following infection with BCG, the normal follicular structure of the red and white pulp is lost and the lymphocytic populations of the white pulp are replaced with sheets of leukocytes
  (MGI Ref ID J:47459)

• abnormal uterine NK cell morphology
  • the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
  (MGI Ref ID J:56503)

• abnormal uterine NK cell physiology
  • decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation
  (MGI Ref ID J:56503)
  • uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
  (MGI Ref ID J:56503)

• decreased susceptibility to parasitic infection
  • Background Sensitivity - unlike mice on a C57BL/6 background, mice on a BALB/c background do not lose weight, show any change in stool consistency, or display heavy parasitic loads in the gastrointestinal tract over the course of a C. parvum infection
  (MGI Ref ID J:50832)

• enlarged spleen
  • develop splenomegaly after infection with BCG
  (MGI Ref ID J:47459)

• increased circulating interleukin-6 level
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased granulocyte number
  • in the blood, bone marrow and spleen following infection with BCG
  (MGI Ref ID J:47459)

• increased leukocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased monocyte cell number
  • following infection with BCG
  (MGI Ref ID J:47459)

• increased susceptibility to bacterial infection
  • following infection with BCG mice develop numerous granulomatous lesions in the liver and necrosis of both the liver and spleen
  (MGI Ref ID J:47459)
  • following infection with BCG mice display an increased bacterial load throughout the infect in contrast to wild-type mice where bacterial numbers peak at 17 days post infection and decline thereafter
  (MGI Ref ID J:47459)

• increased susceptibility to bacterial infection induced morbidity/mortality
  • die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
  (MGI Ref ID J:47459)

• increased uterine NK cell number
  • after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
  (MGI Ref ID J:56503)

• pale spleen
  • spleens become paler as BCG infection proceeds
  (MGI Ref ID J:47459)

mortality/aging

• increased susceptibility to bacterial infection induced morbidity/mortality
  • die by 6 - 10 weeks after infection with the avirulent BCG strain of Mycobacterium bovis
  (MGI Ref ID J:47459)

neoplasm

• altered tumor pathology
  • in C26/Il12 derived tumors, tumor vessels are more numerous and thinner compared to vessels in tumors in wild-type mice
  (MGI Ref ID J:115144)
  • when injected with 5 x 10⁵ C26/Il12 cells only a few mice are able to reject the tumor, in contrast 80 - 100% of wild-type mice reject the tumor
  (MGI Ref ID J:115144)

• decreased tumor latency
  • Normal - however, no difference is detected when parental C26 cells are used
  (MGI Ref ID J:115144)
  • tumor onset is accelerated in 40% of mice injected with 5 x 10⁴ C26 carcinoma cells transduced with Il12 genes (C26/Il12) compared to similarly treated wild-type mice
  (MGI Ref ID J:115144)

reproductive system phenotype

• abnormal maternal decidual layer morphology
  • after gestational day 10 the intercellular composition of the decidua changes suggesting accumulations of fluid and extracellular matrix, areas of necrosis are present and a lack of decidual cellularity is apparent
  (MGI Ref ID J:56503)

• abnormal uterine NK cell morphology
  • the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
  (MGI Ref ID J:56503)

• abnormal uterine NK cell physiology
  • decrease in the number of apoptotic uNK cells in the metrial gland afte day 10 of gestation
  (MGI Ref ID J:56503)
  • uNK cells at implantation sites fail to become heavily granulated and have poorly developed golgi apparati
  (MGI Ref ID J:56503)

• decreased litter size
  • decrease in litter size and increase in the number of resorbed embryos in the first litter
  (MGI Ref ID J:56503)
  • Normal - no difference in litter size or number of resorbed embryos is detected in subsequent pregnancies
  (MGI Ref ID J:56503)
  • phenotype is independent of the genotype of the embryos
  (MGI Ref ID J:56503)

• increased uterine NK cell number
  • after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
  (MGI Ref ID J:56503)

embryo phenotype

• abnormal maternal decidual layer morphology
  • after gestational day 10 the intercellular composition of the decidua changes suggesting accumulations of fluid and extracellular matrix, areas of necrosis are present and a lack of decidual cellularity is apparent
  (MGI Ref ID J:56503)

• abnormal uterine NK cell morphology
  • the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
  (MGI Ref ID J:56503)

• increased uterine NK cell number
  • after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
  (MGI Ref ID J:56503)

endocrine/exocrine gland phenotype

• abnormal uterine NK cell morphology
  • the golgi apparatus is poorly developed, the rough ER is disorganized, and numerous mitochondria are seen in uNK cell at implantation sites at gestational day 12
  (MGI Ref ID J:56503)

• increased uterine NK cell number
  • after day 10 of gestation increased numbers of uNK cells are found in the metrial gland compared to wild-type controls
  (MGI Ref ID J:56503)

hematopoietic system phenotype

• decreased IgG level
  • decrease in the induction of IgG in response to low levels of antigen ((4-hydroxy-3 nitrophenyl)acetyl)
  (MGI Ref ID J:119207)

• decreased IgG2a level
  • following exposure to HgCl2 for 4 weeks, relative to similarly treated wild-type and heterozygous mice
  (MGI Ref ID J:119207)

• increased IgG1 level
  • however, mercury treatment does not result in an increase in IgG1 levels
  (MGI Ref ID J:119207)
  • relative to wild-type controls
  (MGI Ref ID J:119207)

homeostasis/metabolism phenotype

• decreased physiological sensitivity to xenobiotic
  • resistant to mercury induced autoimmune response
  (MGI Ref ID J:119207)

immune system phenotype

• decreased IgG level
  • decrease in the induction of IgG in response to low levels of antigen ((4-hydroxy-3 nitrophenyl)acetyl)
  (MGI Ref ID J:119207)

• decreased IgG2a level
  • following exposure to HgCl2 for 4 weeks, relative to similarly treated wild-type and heterozygous mice
  (MGI Ref ID J:119207)

• decreased susceptibility to autoimmune disorder
  • resistant to mercury induced autoimmune response
  (MGI Ref ID J:119207)

• increased IgG1 level
  • however, mercury treatment does not result in an increase in IgG1 levels
  (MGI Ref ID J:119207)
  • relative to wild-type controls
  (MGI Ref ID J:119207)