eagle-i Harvard UniversityHarvard University
See it in Search
This page is a preview of the following resource. Continue onto eagle-i search using the button on the right to see the full record.


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. 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 B et al, 1996). In both NOD. IFN-gamma -/- and NOD. IFN-gamma - /+ mice, IL-12 administration generates a massive and destructive insulitisand increases the number of pancreatic CD4(+) cells. (Trembleau S 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 S 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 DV et al, 2005).
  2. Related Disease
    Sjogren's syndrome
  3. Related Disease
    type 1 diabetes mellitus
  4. Related Publication or Documentation
    Multiple defects of immune cell function in mice with disrupted interferon-gamma genes.
  5. Related Publication or Documentation
    Diabetes acceleration or prevention by a coxsackievirus B4 infection: critical requirements for both interleukin-4 and gamma interferon.
  6. 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.
  7. Related Publication or Documentation
    Genetic absence of gamma-interferon delays but does not prevent diabetes in NOD mice.
  8. 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.
  9. Parental Strain Name
    B6;129 segregating background
  10. Genetic Alteration(s)
    Interleukin 4 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 histocompatibility complex class II antigens.
  14. Phenotype Findings
    Increased time to onset for diabetes.
  15. Location
    Genetically Modified NOD Mouse Core Facility (HMS)
Provenance Metadata About This Resource Record

Copyright © 2016 by the President and Fellows of Harvard College
The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016