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eagle-i ID


Resource Type

  1. Mus musculus


  1. Resource Description
    Development: A neomycin expression cassette was inserted into exon 3 of Ctla4 (cloned from 129/Sv) and transfected into R1 (129X1/SvJ x 129S1/Sv)F1-Kitl+ embryonic stem cells. These ES cells were injected into C57BL/6 background. (Chambers CA et al, 1997). Luhder F et al subsequently backcrossed this mutation to NOD/LtJ. The line is currently at the 31th backcross (2005). CTLA-4 deficient mice are viable, fertile, and normal in size but develop a fatal lymphoproliferative disorder. All homozygous mice on various backgrounds, including C57BL/6, BALB/c, and 129SV die at 3-4 weeks of age due to massive polyclonal expansion of T-cells and massive lymphocyte infiltration into non-lymphoid organs, such as heart, liver, lung and pancreas. On NOD/LtJ background, CTL4 deficient mice die around 3 weeks of age of massive lymphocyte proliferation and infiltration into multiple organs, or of hyperacute diabetes when crossed to a pancreas-reactive TCR transgene. (Luhder et al, 2000).
  2. Related Disease
    type 1 diabetes mellitus
  3. Related Publication or Documentation
    Lymphoproliferation in CTLA-4-deficient mice is mediated by costimulation-dependent activation of CD4+ T cells.
  4. Related Publication or Documentation
    Pinpointing when T cell costimulatory receptor CTLA-4 must be engaged to dampen diabetogenic T cells.
  5. Parental Strain Name
  6. Genetic Alteration(s)
    CTLA 4 deletion
  7. Clinical or Environmental Source
    Controlled Facility at Jackson labs
  8. Phenotype Findings
    Develop a fatal lymphoproliferative disorder.
  9. Location
    Genetically Modified NOD Mouse Core Facility (HMS)
Provenance Metadata About This Resource Record

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The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016