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Use of genetic knockouts to modulate disease expression in a murine model of lupus, MRL/Ipr mice

Authors
  • Reilly, Christopher M.1, 2
  • Gilkeson, Gary S.1, 2
  • 1 Medical University of South Carolina, Medical Research Service, Ralph H. Johnson VAMC, 96 Jonathon Lucus St. Suites 912, Charleston, SC, 29425 , Charleston
  • 2 Medical University of South Carolina, Department of Medicine, 96 Jonathon Lucus St. Suite 912, Charleston, SC, 29425 , Charleston
Type
Published Article
Journal
Immunologic Research
Publisher
Humana Press
Publication Date
Apr 01, 2002
Volume
25
Issue
2
Pages
143–153
Identifiers
DOI: 10.1385/IR:25:2:143
Source
Springer Nature
Keywords
License
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Abstract

MRL-MPJ Fas1pr (MRL/lpr) mice are a prototypic murine model for lupus characterized by an accelerated autoimmune syndrome. Disease begins as early as 8-wk-of-age in these animals with polyclonal B cell activation and elevated levels of serum IgM. By 12 to 16-wk-or-age MRL/lpr mice begin to produce a variety of autoantibodies including anti-dsDNA and anti-ss-DNA antibodies. From 16 to 24 wk, MRL/lpr mice develop proliferative immune complex mediated glomerulonephritis, vasculitis, arthritis, and massive lymphadenopathy that results in ren al failure and death in 50% of the mice by 24-wk-of-age. This review will discuss several different genetic knockout experimental approaches used to study disease expression in MRL/lpr mice including various approaches in our laboratory aimed at autoantibody (Ab) production and inflammatory mediators.

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