Homozygous Ch25h (cholesterol 25-hydroxylase) knock-out mice have increased levels of IgA and may be useful in studies innate and adaptive immune system interactions.
Dr. David Russell, Univ of Texas Southwest Med Ctr Dallas
Stimulation of toll-like receptors has been shown to normally induce the expression of Ch25h (cholesterol 25-hydroxylase) in macrophages. Il2 (interleukin 2)-mediated stimulation of B cell proliferation is suppressed, activation-induced cytidine deaminase (AID) expression is repressed, and immunoglobulin class switch recombination is blocked, leading to markedly decreased IgA production.
The Ch25h gene was deleted in this targeted mutant strain. Homozygotes have excessive levels of IgA in their sera, mucosa, and the bronchial fluid of the lungs. This strain may be useful in studies of innate immune system regulation of adaptive immune responses.
The intron-less gene was deleted in its entirety and replaced by the PolII neo pA expression cassette in 129S6/SvEvTac-derived SM1 embryonic stem (ES) cells. This strain was backcrossed to C57BL/6J for more than 10 generations by the donating laboratory.
|Allele Name||targeted mutation 1, David W Russell|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Ch25h, cholesterol 25-hydroxylase|
|Strain of Origin||129S6/SvEvTac|
|Molecular Note||The intron-less gene was deleted in its entirety and replaced by the PolII neo pA expression cassette. The absence of protein expression was confirmed by western blot analysis on lung and liver extracts after Kdo2-Lipid A induction.|
When using the Ch25h- mouse strain in a publication, please cite the originating article(s) and include JAX stock #016263 in your Materials and Methods section.