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Transgenic expression of a soluble complement inhibitor protects against renal disease and promotes survival in MRL/lpr mice.
Complement and autoimmune glomerular diseases.
Administration of a soluble recombinant complement C3 inhibitor protects against renal disease in MRL/lpr mice.
C5a promotes development of experimental lupus nephritis which can be blocked with a specific receptor antagonist.
CR1/CR2 deficiency alters IgG3 autoantibody production and IgA glomerular deposition in the MRL/lpr model of SLE.
TNF is a key mediator of septic encephalopathy acting through its receptor, TNF receptor-1.
Lupus: The microbiome angle.
Nephrology Research Training Grant