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lüll The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus Liphaus BL; Kiss MHClinics (Sao Paulo) 2010[Mar]; 65 (3): 327-33Systemic lupus erythematosus is a prototypical autoimmune disease characterized by the deregulation of T and B cells, tissue infiltration by mononuclear cells, tissue damage and the production of autoantibodies. There is a consensus that accelerated apoptosis of circulating lymphocytes and/or impaired clearance of apoptotic bodies may increase the amount of nuclear antigens presented to T lymphocytes. This process is accompanied by autoimmune responses that can lead to the development of lupus. The dysfunction of apoptosis may be a direct consequence of alterations in proteins/genes such as Fas, Bcl-2 and C1q. Increased expression of Fas antigen could intensify the exposure of hidden antigens. The overexpression of Bcl-2 protein might inhibit the removal of auto-reactive cells, and the lack of C1q could impair the clearance of self-antigens. The complete knowledge of the role of apoptosis components in the etiopathogenesis of lupus could lead to the development of new therapies targeting the apoptotic threshold, which could result in a more specific and effective disease response compared to global immunosuppression. This review summarizes the role of each component of the apoptotic process in the pathogenesis of lupus.|Apoptosis/*immunology[MESH]|Complement C1q/deficiency/*immunology[MESH]|Fas Ligand Protein/*immunology/metabolism[MESH]|Humans[MESH]|Lupus Erythematosus, Systemic/*etiology/immunology[MESH]|Proto-Oncogene Proteins c-bcl-2/*immunology/metabolism[MESH] |