Abstract
Abstract Sle1 is a potent susceptibility locus for spontaneous systemic autoimmunity derived from the NZM2410 mouse strain. The NZW-derived suppressive modifier locus, Sles1, specifically prevents the spontaneous loss in tolerance mediated by the B6.Sle1 congenic. Fine mapping combined with phenotypic characterization of series of recombinant mouse strains have mapped Sles1 to an approximately 638 KB segment on murine chromosome 17. This revealed extensive epistatic gene interactions within the Sles1 region and suggested Btnl2 and H2 genes as the strongest candidates. We have performed targeted resequencing on B6 and B6.Sles1 mice and have identified functional polymorphisms within the Sles1 interval between the two mice strains. We further generated a series of BAC transgenic mice and have performed RNA-seq analysis and cell surface expression studies on B cells, Bone-marrow derived macrophages and Bone-marrow derived dendritic cells. We are in the process of aging BAC transgenic mice and will be phenotyping all the mice at 7 months with a goal to identify one or more genes driving the pathogenesis of autoimmunity.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
