Table 1.

Comparision of mouse models of SLE and lupus nephritis

	Clinical	Histologic	autoantibodies
MRLlpr	Prominent lymphoadenopathy 50% mortality by 24 weeks Death due to GN Polyarthritis Dermatitis	Mesangial and endothelial proliferation Mesangial and sub-endothelial IgG and C3 deposition Monocytic infiltrate	High-titer ANA IgG and IgM anti-DNA IgM and IgG rheumatoid factor Anti-Ro and La
NZB/NZW F1 NZM2410	Splenomeagly 50% mortality at 8 months in females Death due to GN	Mesangial and endothelial proliferation Mesangial and sub-endothelial IgG and C3 deposition glomerular and tubular proteinaceous deposits Monocytic infiltrate	IgG anti-DNA, especially lgG2a and 2b IgG anti-chromatin IgG anti-phospholipid
BXSB	50% mortality in males at 5 months Females have late-onset disease Death due to GN Lymphoadenopathy, but not as significant as MRLlpr mice	Exudative nephritis PMN infiltrate Mesangial and capillary IgG and C3 deposition Tublo-interstitial IgG deposition	Anti-dsDNA and chromatin IgG High levels of circulating immune complexes Speckled ANA due to anti-nucleolar staining
B6.Fcgr2b−/−	50% mortality at 9 months in females males have normal lifespan Death due to GN Lung vasculitis in 30% to 40% of female mice	Endothelial proliferation Thickening of mesangium and glomerular basement membrane Glomerular fibrosis Monocytic and B cell infiltrate	Anti-DNA and chromatin IgM and IgG in particular lgG2b and 2c
Pristane	No mortality related to glomerulonephritis Female mice more susceptible Arthritis Hemorrhage in lung	Focal to global proliferative lesions Mesangial and sub-endothelial IgM, IgG, and C3 deposits	IgG anti-RNP IgM anti-DNA Moderate ANA development