Abstract
In DDD, fluid-phase dysregulation of the AP of the complement cascade leads to deposition of complement activation products (iC3b, C5, C6, C7, C8, C9) along the GBM. Our data show that a soluble form of the transmembrane complement regulator sCR1 prevents abnormal hemolysis in vitro in presence C3Nefs. In addition, its administration to DDD mouse models results in restoration of plasma C3 levels and reduction of C3 deposition along the GBM. Similar therapeutic effects have been seen using human or mouse purified factor H in DDD mouse models.4,5
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