Mice homozygous for Stat6tm1Gru show a striking defect in the generation of Th2 cells; lymphocytes fail to proliferate in response to IL-4. These mice may be useful for studies of colitis and other inflammatory diseases.
Dr. Michael J. Grusby, Harvard Medical School
Mice homozygous for the Stat6tm1Gru mutation show a striking defect in the generation of Th2 cells. Lymphocytes are unable to respond to IL4 as measured in a variety of in vitro and in vivo assays. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. Mesenteric lymph node cells from STAT6-/- mice with colitis exhibited reduced secretion of IL-4, IL-5, IL-13, and IFN-gamma. They also show impaired Th2 differentiation and reduced airway response to allergen. With enhanced renal injury, Th1 and Th17 nephritogenic immune responses were increased in STAT6-/- mice while production of IL-5, a key Th2-associated cytokine, was decreased significantly.
|Allele Name||targeted mutation 1, Michael J Grusby|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||S6KO; Stat6-|
|Gene Symbol and Name||Stat6, signal transducer and activator of transcription 6|
|Strain of Origin||129S2/SvPas|
|Molecular Note||The region encoding the SH2 domain, which is essential for dimerization, was replaced by the insertion of a neomycin selection cassette. Immunoblot analysis of lysates from the spleens and thymi of homozygous mutant mice showed an absence of encoded protein.|
|Mutations Made By|| |
Dr. Michael Grusby, Harvard Medical School
When using the Stat6- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002828 in your Materials and Methods section.