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Immunol Res. 2002;25(2):143-53.

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

Author information

1
Medical Research Service, Ralph H. Johnson VAMC, Charleston, SC, USA. reillycm@musc.edu

Abstract

MRL-MPJ Fas(lpr) (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-of-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 renal 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.

PMID:
11999168
[Indexed for MEDLINE]

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