Key result
NOS2-deficient MRL-lpr/lpr mice developed similar glomerular and synovial pathology to wildtype mice, but had significantly less vasculitis of medium-sized renal vessels and lower IgG rheumatoid factor.
Population
MRL-lpr/lpr mice (autoimmune syndrome model)
Comparison
Targeted disruption of NOS2 vs Wildtype (+/+) MRL-lpr/lpr mice
Design
Preclinical
Authors
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Indicates heterogeneous NOS2 dependence across lupus manifestations; hypothesis-generating for selective targeting and leaves open validation in other models.
Targeted disruption of NOS2 in MRL-lpr/lpr mice reduces renal vasculitis and IgG rheumatoid factor levels but does not affect glomerular or synovial pathology, indicating heterogeneity in disease mechanisms.
Gilkeson et al. (1997) studied Autoimmune syndrome. Targeted disruption of NOS2 vs. Wildtype (+/+) MRL-lpr/lpr mice was evaluated on Glomerular and synovial pathology, vasculitis, and autoantibody levels. NOS2-deficient MRL-lpr/lpr mice developed similar glomerular and synovial pathology to wildtype mice, but had significantly less vasculitis of medium-sized renal vessels and lower IgG rheumatoid factor.
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