The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
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.
| Main Authors: | , |
|---|---|
| Format: | Digital revista |
| Language: | English |
| Published: |
Faculdade de Medicina / USP
2010
|
| Online Access: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1807-59322010000300014 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|