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 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 de...
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 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.
This Il2tm1Hor deficient strain was developed in the lab of Dr. Ivan Horak at the Institute for Virology and Immunobiology at the Univerity of Wurzburg. The 129-derived E14 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
When maintaining a live colony, heterozygous mice may be bred to wildtype mice from the colony or to C57BL/6J inbred mice (Stock No. 000664). Homozygous mice die by 3-5 weeks of age due to hemolytic anemia.
|Please inquire about possible genotypes.|
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