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eagle-i ID


Resource Type

  1. Mus musculus


  1. Resource Description
    Development: The targeting vector has a neomycin resistance gene inserted into exon 2, which introduces a terminaison codon after the first 30 amino acids of the mature IFN-gamma protein. The targeting vector was transferred into AB-1 embryonic stems. (Dalton et al,1993). The mutation was then transferred to the NOD background (Wang B et al, Mathis D, 1997). The line is currently at the 7th backcross in NOD/LTJ (2008). Deficient mice develop normally and are healthy in the absence of pathogens. NOD Mice homozygous for the IFN-gamma KO targeted mutation are viable and fertile. The genetic absence of IFN-gamma does not prevent either insulitis or diabetes in the NOD mice, but increases the time to onset. Splenocytes taken from IFN-gamma deficient 3 diabetic mice are fully capable of transferring diabetes to naive recipients (Hultgren et al,1996). In both NOD. IFN-gamma -/- and NOD. IFN-gamma - /+ mice, IL-12 administration generates a massive and destructive insulitis and increases the number of pancreatic CD4(+) cells (Trembleau et al, 2003). NOD IFN-gamma 0 homozygous mice do not display increased acinar cell apoptosis and abnormal salivary protein expression, typically observed in parental NOD mice prior to Sjogren's syndrome-like autoimmune exocrinopathy (Cha et al, 2004). When NOD. IFN-gamma -/- mice are infected with Coxsackievirus B4, Insulitis or diabetes development is delayed by several weeks compared to NOD mice. When mice are infected at 12 weeks of age, neither acceleration nor long-term protection is elicited in NOD IFN-gamma - /- mice (Serreze et al, 2005).
  2. Related Disease
    type 1 diabetes mellitus
  3. Related Publication or Documentation
    Multiple defects of immune cell function in mice with disrupted interferon-gamma genes.
  4. Related Publication or Documentation
    Diabetes acceleration or prevention by a coxsackievirus B4 infection: critical requirements for both interleukin-4 and gamma interferon.
  5. Related Publication or Documentation
    IL-12 administration accelerates autoimmune diabetes in both wild-type and IFN-gamma-deficient nonobese diabetic mice, revealing pathogenic and protective effects of IL-12-induced IFN-gamma.
  6. Related Publication or Documentation
    Genetic absence of gamma-interferon delays but does not prevent diabetes in NOD mice.
  7. Related Publication or Documentation
    A dual role for interferon-gamma in the pathogenesis of Sjogren's syndrome-like autoimmune exocrinopathy in the nonobese diabetic mouse.
  8. Related Publication or Documentation
    Interferon-gamma impacts at multiple points during the progression of autoimmune diabetes.
  9. Parental Strain Name
  10. Genetic Alteration(s)
    Gamma Interferon deletion
  11. Clinical or Environmental Source
    Controlled facility at Jackson labs
  12. Phenotype Findings
    Impaired production of macrophage antimicrobial products.
  13. Phenotype Findings
    Reduced expression of macrophage major histo-compatibility complex class II antigens.
  14. 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