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 first exon of IL10 was disrupted after the fourth codon, a neomycin resistance cassette, and an additional termination codon in the third exon, was used for homologous recombination in E14-1 ES cells (129P2/OlaHsd-derived) (Kuhn R et al, Muller W, 1993). The mutation was then transferred to the NOD/Lt background using a marker assisted protocol (Serreze DV et al, Rabinovitch A, 2001). NOD/Lt mice heterozygous for this IL100 allele and homozygous for diabetes susceptibility loci (Idd) were intercrossed to develop mice homozygous for IL10tm1Cgn and all Idd loci. The line is currently at the 11th backcross to NOD/LtJ (2005). Used to study gamma interferon. Mice homozygous for the IL10 targeted mutation are viable and fertile when housed under SPF conditions.
  2. Related Disease
  3. Related Disease
    type 1 diabetes mellitus
  4. Related Publication or Documentation
    Th1 to Th2 cytokine shifts in nonobese diabetic mice: sometimes an outcome, rather than the cause, of diabetes resistance elicited by immunostimulation.
  5. Parental Strain Name
  6. Genetic Alteration(s)
    Interleukin 10 deletion
  7. Clinical or Environmental Source
    Controlled Facility at Jackson labs
  8. Phenotype Findings
    This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain.
  9. Phenotype Findings
    The IL10 mutation also renders this line susceptible to colitis (although not as severe as other strains of IL10 deficient mice when maintained under standard housing conditions).
  10. 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