Incomplete clearance of apoptotic cells in systemic lupus erythematosus: pathogenic role and potential biomarker

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with repeated inflammation against multiple organs. Although its pathophysiology is not yet unveiled, uncleared apoptotic cells and their accumulation in tissue contribute to the autoimmune disturbance in SLE. Apoptosis is a programmed cell death process, which maintains tissue homeostasis and inhibits the development of any further immune response against apoptotic remnants. Earlier studies revealed that various 'eat-me' signals on apoptotic cells, bridging molecules and their receptors on phagocytes play a role in such a complicated process. Tyro3-Axl-Mer receptors, their bridging molecules, milk fat globulin epidermal growth factor-8, T-cell immunoglobulin mucin domain protein family, scavenger receptors, C1q, and pentraxins were found to be abnormal in SLE. In this review, apoptosis and clearance of its remnants are summarized, and the molecules involved in the incomplete clearance of apoptotic cells in SLE are discussed.