Homozygous mutant mice 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. Homozygotes show an atrophied pancreas with apparently intact islets. These mice may be useful in studies aimed at the manipulation of the immune response.
Dr. Ivan Horak, Forschungs institut fur Molekulare
Homozygous mutant mice 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 wild-type. 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 C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between six 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 three to five weeks postnatally of a form of hemolytic anemia.
This mutant strain was developed in the lab of Dr. Ivan Horak at the Institute for Virology and Immunobiology at the Univerity of Wurzburg. The 129P2/OlaHsd-derived E14 embryonic stem (ES) cell line was used.
|Allele Name||targeted mutation 1, Ivan Horak|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||IL-2 KO; IL-2-; IL-2null; Il2-|
|Gene Symbol and Name||Il2, interleukin 2|
|Gene Synonym(s)||IL-2; Il-2; TCGF; lymphokine|
|Strain of Origin||129P2/OlaHsd|
|General Note||Phenotypic Similarity to Human Syndrome: Inflammatory Bowel Disease (J:15223).Phenotypic Similarity to Human Syndrome: Inflammatory Bowel Disease (J:51450) with B2m |
|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
(het x het) and (het x wt) matings Expected coat color from breeding:Black
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