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Review
. 2010 Mar;65(3):327-33.
doi: 10.1590/S1807-59322010000300014.

The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus

Affiliations
Review

The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus

Bernadete L Liphaus et al. Clinics (Sao Paulo). 2010 Mar.

Abstract

Systemic 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.

Keywords: Apoptosis; Bcl-2 protein; C1q complement component; Fas protein; Systemic Lupus Erythematosus.

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