Phenotypes Associated with This Genotype

Genotype
MGI:5298853

• Allelic Composition: Cd59a^tm1Bpm/Cd59a^tm1Bpm
• Genetic Background: B6.129-Cd59a^tm1Bpm

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

renal/urinary system

increased renal tubule apoptosis ( J:92414 )

• following ischemic reperfusion injury

increased susceptibility to kidney reperfusion injury ( J:92414 )

• following ischemic reperfusion injury, mice exhibit more severe tubular damage, greater lymphocyte infiltration, increased tubular apoptosis, increased deposition of C9, and fail to recover compared with wild-type mice

immune system

decreased B cell proliferation ( J:119703 )

• following stimulation with LPS or anti-CD40 antibodies

increased T cell proliferation ( J:122201 )

• in CD4+ T cells stimulated in vitro or in vivo with recombinant vaccinia virus glycoprotein 13 (p13)

• in CD4+ T cells stimulated with anti CD3 antibodies and antigen presenting cells

• however, proliferation in response to anti-CD3 and anti-CD28 antibodies is normal

increased double-positive T cell number ( J:123582 )

• in the lungs of influenza-infected mice originating from the thymus

increased neutrophil cell number ( J:123582 )

• in the lungs of influenza-infected mice

decreased plasma cell number ( J:119703 )

• following stimulation with sheep red blood cells

increased CD4-positive, alpha-beta T cell number ( J:123582 )

• in the lungs of influenza-infected mice

abnormal CD4-positive, alpha-beta T cell physiology ( J:119703 , J:123582 )

• CD4+ T cells exhibit decreased ability to activate B cells compared with wild-type T cells (J:119703)

• CD4+ T cells from influenza-infected mice exhibit increased influenza-specific activation (J:123582)

abnormal humoral immune response ( J:119703 )

• reduced in response to stimulation with sheep red blood cells

decreased IgG level ( J:119703 )

• all sub-classes of anti-sheep red blood cell IgG following second immunization

abnormal complement pathway ( J:92414 )

• following ischemic reperfusion injury, mice exhibit a greater accumulation of C9 in the kidneys compared with wild-type mice

increased susceptibility to experimental autoimmune myasthenia gravis ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis, mice exhibit a mild decreased grip strength and worse clinical scores compared with wild-type mice

myositis ( J:113567 )

• some following induction of experimental autoimmune myasthenia gravis

lung inflammation ( J:123582 )

• following infection with influenza

decreased susceptibility to Poxviridae infection ( J:122201 )

• mice infected with recombinant vaccinia virus exhibit lower viral titers 3 days post-infection compared with wild-type mice

increased susceptibility to Orthomyxoviridae infection ( J:123582 )

• mice infected with influenza exhibit increased lung pathology (the degree of haemorrhage, interstitial leukocyte infiltration (neutrophil, CD4+ T cell, and CD4+CD8+ T cells), and perivascular lymphoid aggregation), mild fibrosis, and increased complement-independent deposition of membrane attack complex in the respiratory airways compared with wild-type mice

cellular

increased renal tubule apoptosis ( J:92414 )

• following ischemic reperfusion injury

decreased B cell proliferation ( J:119703 )

• following stimulation with LPS or anti-CD40 antibodies

increased T cell proliferation ( J:122201 )

• in CD4+ T cells stimulated in vitro or in vivo with recombinant vaccinia virus glycoprotein 13 (p13)

• in CD4+ T cells stimulated with anti CD3 antibodies and antigen presenting cells

• however, proliferation in response to anti-CD3 and anti-CD28 antibodies is normal

homeostasis/metabolism

increased susceptibility to kidney reperfusion injury ( J:92414 )

• following ischemic reperfusion injury, mice exhibit more severe tubular damage, greater lymphocyte infiltration, increased tubular apoptosis, increased deposition of C9, and fail to recover compared with wild-type mice

hematopoietic system

decreased B cell proliferation ( J:119703 )

• following stimulation with LPS or anti-CD40 antibodies

increased T cell proliferation ( J:122201 )

• in CD4+ T cells stimulated in vitro or in vivo with recombinant vaccinia virus glycoprotein 13 (p13)

• in CD4+ T cells stimulated with anti CD3 antibodies and antigen presenting cells

• however, proliferation in response to anti-CD3 and anti-CD28 antibodies is normal

increased double-positive T cell number ( J:123582 )

• in the lungs of influenza-infected mice originating from the thymus

increased neutrophil cell number ( J:123582 )

• in the lungs of influenza-infected mice

decreased plasma cell number ( J:119703 )

• following stimulation with sheep red blood cells

increased CD4-positive, alpha-beta T cell number ( J:123582 )

• in the lungs of influenza-infected mice

decreased IgG level ( J:119703 )

• all sub-classes of anti-sheep red blood cell IgG following second immunization

abnormal CD4-positive, alpha-beta T cell physiology ( J:119703 , J:123582 )

• CD4+ T cells exhibit decreased ability to activate B cells compared with wild-type T cells (J:119703)

• CD4+ T cells from influenza-infected mice exhibit increased influenza-specific activation (J:123582)

behavior/neurological

decreased grip strength ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis

muscle

myositis ( J:113567 )

• some following induction of experimental autoimmune myasthenia gravis

cardiovascular system

choroidal neovascularization ( J:143638 )

• in response to laser treatment, mice exhibit severe choroid neovasculatization with deposition of membrane attack complex compared with wild-type mice

vision/eye

choroidal neovascularization ( J:143638 )

• in response to laser treatment, mice exhibit severe choroid neovasculatization with deposition of membrane attack complex compared with wild-type mice

respiratory system

lung inflammation ( J:123582 )

• following infection with influenza

pulmonary fibrosis ( J:123582 )

• mild following infection with influenza