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Considerable evidence points to a dysregulated or dysfunctional clearance of apoptotic cells in human SLE
Apoptosis, or programmed cell death is central in the normal physiological function of multicellular organisms and is implicated in developmental and homoeostatic mechanisms. It is a complex process that seeks to limit the ability for cellular constituents to leak from a cell and cause damage to surrounding tissues, and to prevent intracellular material from being recognised by the immune system. Phagocytosis of apoptotic cells is critical in their disposal and occurs before membrane degradation, thus ensuring the rapid and safe elimination of potentially inflammatory or immunogenic material from the circulation.
Since the pioneering work by Rosen and colleagues first demonstrated that an autoantigen associated with systemic rheumatic diseases could be located in the blebs of apoptotic cells,1 there has been a growing interest in the role of apoptosis in the production of autoantibodies. It has subsequently been shown that many such autoantigens can be found in macromolecular structures in cell surface vesicles during apoptosis.2,3 These possess the antigenic determinants that bind to autoantibodies from patients with a variety of autoimmune diseases.4,5 However, it must be appreciated that because apoptosis is a normal physiological event, exposure to potential autoantigens is likely to be common in healthy subjects without the induction of autoimmunity. As more is understood about the process of apoptosis, the potential for dysregulation at multiple levels leading to the induction of autoimmune diseases is suggested (fig 1). It is likely that further research will uncover more of these links.
One area of research which has attracted interest is concerned with …