Genetic models for the clearance of apoptotic cells.

The immunogenic potential of nuclear antigens exposed during apoptosis, together with considerable animal data suggesting that impaired apoptotic clearance can result in systemic lupus erythematosus (SLE)-like autoimmunity, has lent support to the idea that self-immunization with apoptotic debris is a key driving mechanism in lupus. The multiple roles of complement receptors, diverse scavenger receptors, and intermediate proteins that bind to and opsonize apoptotic cells indicate a complex web of interactions leading to the clearance of apoptotic debris. Disturbances in parts of this system may lead to lupus or to lupus exacerbations. Therapy directed toward augmenting clearance and decreasing concomitant inflammation may lead to improved management of SLE.