Decay-accelerating factor but not CD59 limits experimental immune-complex glomerulonephritis.

摘要: The complex balance between the pro-activating and regulatory influences of complement system can affect pathogenesis immune complex-mediated glomerulonephritis (ICGN). Key proteins include decay accelerating factor (DAF) CD59, which inhibit C3 activation C5b-9 generation, respectively. Both are glycosylphosphatidylinositol-linked cell membrane proteins, widely distributed in humans mice. Chronic serum sickness induced by daily immunization with horse spleen apoferritin over 6 weeks was used to induce ICGN DAF-, CD59- DAF/CD59-deficient mice, wild-type littermate mice serving as controls. DAF had an increased incidence GN relative controls associated significantly glomerular deposition. Disease expression CD59-deficient no different than DAF- also monocyte chemoattractant protein-1 mRNA infiltration CD45+ leukocytes. Our findings suggest that is strongly experimental while downstream formation lesser pathogenic importance this model.