These IL-2 knock-out mice exhibit an impaired response to polyclonal T cell activators, deficits in their helper function, and a reduction in natural killer cell activity.
Dr. Ivan Horak, Forschungs institut fur Molekulare
Homozygous mutant mice for the Il2tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the BALB/c, C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the JAX Notes Fall 1996 article.
|Allele Name||targeted mutation 1, Ivan Horak|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||IL-2-; Il2-; IL-2 KO; IL-2null|
|Gene Symbol and Name||Il2, interleukin 2|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||Insertion of a neomycin-resistance gene into the third exon introduced several stop codons in all reading frames.|
|Mutations Made By|| |
Dr. Ivan Horak, Forschungs institut fur Molekulare
When maintaining a live colony, heterozygous mice may be bred to wildtype siblings, or to C3H/HeJ inbred mice (Stock No. 000659).
When using the IL-2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002228 in your Materials and Methods section.
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