Inflammatory clearance of apoptotic remnants in systemic lupus erythematosus (SLE).

Deficiencies in the recognition and phagocytosis of dead and dying cells have been shown to be one of the main alterations in patients with systemic lupus erythematosus (SLE). Cellular as well as humoral elements play an important role in the clearance of apoptotic and necrotic cells. Non-ingested nuclear material may provide survival signals for autoreactive B-cells and consequently antibodies directed against nuclear structures will be produced. In healthy individuals, nuclear fragments are not phagocytosed in whole blood. Instead, they are mainly degraded by the action of plasma DNases and complement factors. In contrast, the uptake of nuclear fragments by blood-borne phagocytes is increased in most patients with SLE. The phagocytosis of this kind of prey, which might be opsonised by autoantibodies, may contribute to the maintenance of inflammatory responses in SLE.