C3 and autoimmune polyendocrinopathy: In addition to opsonising apoptotic cells, C3 binding to B2GPI provides a binding site for factor H which then mediates degradation of C3 via the activity of factor I. There are suggestions that complement dysregulation plays a part in APS as evidenced by data from mouse models of APS showing that inhibition of C3 activity can prevent fetal loss [12,13].