الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
SLE is a systemic autoimmune disease that results from interaction of genetic and environmental factors which together promote autoantibody production directed prominently to nuclear macromolecules. Since the nuclear molecules can have intrinsic immunological activity, the resulting immune complexes can cause potent stimulation of the immune system.
The pathogenesis of SLE is critically dependent on the formation of immune complexes whose antigenic components can derive from dead and dying cells. The levels of these components may rise because of impairment of the cellular and humoral immune systems involved in the clearance of dead and dying cells. In the presence of extracellular nuclear antigens, immune complexes can form with antibodies to DNA and other nuclear molecules; this figure depicts the DNA system.
Several evidences indicate that abnormalities in the apoptosis (programmed cell death) process could be related to development of SLE.
The importance of apoptosis in immune tolerance wasproved in a study of the genetic defects in FAS and itsligand (FASL) in mouse models of human SLE.
FAS/FAS ligand system is the main extrinsic pathway for the initiation of apoptosis in numerous cells and tissues.
FAS is a membrane protein of the transmembrane tumor necrosis factor superfamily of death receptors and plays an important role in apoptotic signaling in different cells. Thisreceptor induces apoptosis by binding to its natural ligand.
FASL is a member of tumor necrosis factor superfamily and initiates the death signal cascade, which ultimately results in apoptotic cell death. Although FAS is existing constitutively on the surface of resting cells in low levels, it is expressed prominently on the surface of activated T cells.