C.129S6(Cg)-Ccl11^tm1Mer/J

Stock number: 017618
Research areas: Hematological Research, Immunology, Inflammation and Autoimmunity Research

Description

These Ccl11 knockout mice exhibit a reduced total eosinophil count in peripheral blood and may be useful for studying eosinophilia and inflammatory disorders.

Detailed description

Mice homozygous for the Ccl11^tm1Mer allele contain a neomycin resistance cassette that replaces exon 2 and part of exon 3, abolishing gene expression. CCL11 (or eotaxin) is an eosinphil specific C-C chemokine involved in eosinophil recruitment. Mice deficient in eotaxin exhibit a reduced total eosinophil count in peripheral blood. Following antigen challenge, eosinophils are significantly reduced in the early, but not late, phase of the inflammatory response. Homozygotes are viable, fertile, normal in size, and do not display any gross physical abnormalities. These mice may be useful for studying eosinophilia in peripheral blood and inflammatory disorders.

Development

A targeting vector containing a PGKneo cassette was used to disrupt all of exon 2, which encodes the mature protein, and most of exon 3. The construct was electroporated into 129S6/SvEvTac-derived TC1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The resulting chimeric animals were crossed to outbred mice and maintained on a mixed background.

Allele

Symbol: Ccl11^tm1Mer
Name: targeted mutation 1, Marc E Rothenberg
MGI accession ID: MGI:2384435
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: eotaxin-; eotaxin-1; Eot^-
Marker symbol: Ccl11
Marker name: chemokine (C-C motif) ligand 11
Chromosome: 11
Strain of origin: 129S6/SvEvTac
Molecular note: All of exon 2 and the majority of exon 3 were replaced by a neomycin selection cassette. In addition to containing the 3' UTR, the deleted region encoded most of the mature protein. Transcript was undetected in homozygous mutant mice via Northern blot analysis of skin and lung RNA (the latter of which was isolated from mice treated with and subsequently challenged with OVA).