The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
Clinics
;
65(3): 327-333, 2010.
Article
in English
| LILACS
| ID: lil-544025
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.
Full text:
Available
Index:
LILACS (Americas)
Main subject:
Complement C1q
/
Apoptosis
/
Fas Ligand Protein
/
Lupus Erythematosus, Systemic
Limits:
Humans
Language:
English
Journal:
Clinics
Journal subject:
Medicine
Year:
2010
Type:
Article
Affiliation country:
Brazil
Institution/Affiliation country:
Universidade de São Paulo/BR
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