Lupus nephritis
The role of apoptosis and removal of apoptotic cells in the genesis of systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease with an unknown aetiology that is characterized by the production of autoantibodies against nuclear components, such as DNA, histones and nucleosomes. Many studies report a role of aberrant apoptosis in the development of SLE, which may be the result of an increased rate of apoptosis, or apoptosis at the wrong time or place. In addition, insufficient clearance of apoptotic cells and debris may explain the development of SLE. The accumulation of apoptotic cells may result from defects in recognition of apoptotic cells by phagocytes, opsonins or their receptors, or simply from a reduced intrinsic phagocytic capacity of phagocytes. When apoptosis exceeds the clearance capacity, apoptotic blebs will segregate and autoantigens with apoptosis-induced modifications will be released. This released apoptotic cell debris can be taken up by professional antigen presenting cells, such as dendritic cells. These cells will present modified autoantigens in an immunogenic fashion to T cells, which subsequently activate autoantibody producing B cells. In summary, development of SLE may be the result of aberrant apoptosis and/or decreased clearance of apoptotic material by phagocytes.