Table 2 |.

Animal models of NPSLE

Mouse model	Advantages	Disadvantages
MRL/MpJ-Faslpr/lpr	Rapid onset, multisystemic presentation akin to SLE in patients Available congenic controls	Complex pathogenic contributors
NZB × NZW F1 offspring	Neuropsychiatric disease occurs before systemic disease Slow progression is an approximation of human disease Appropriate brain regions are affected	Delayed progression limits feasibility of certain studies Unclear contribution of neuroprogenitor cells in the corpus callosum
564Igi	Emphasizes the contribution of a particular anti-nuclear antibody (directed against RNA) and increased type I interferon activity to disease development	Minimizes effects of the adaptive immune response due to an invariant IgG clone
C57Bl/6-Faslpr/lpr	The same Fas mutation as in MRL/lpr mice, but on the C57Bl/6 background, which allows for more effective genetic manipulation using existing mutant strains	Disease develops in an attenuated fashion and with incomplete penetrance compared with that in MRL/lpr mice

IgG, immunoglobulin G; NPSLE, neuropsychiatric systemic lupus erythematosus; NZB, New Zealand black; NZW, New Zealand white; SLE, systemic lupus erythematosus. Other models of SLE with neuropsychiatric disease exist but are less often employed owing to various confounding variables, such as anatomical abnormalities or technical considerations.