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

Detalhes bibliográficos
Autor(a) principal: Liphaus, Bernadete L.
Data de Publicação: 2010
Outros Autores: Kiss, Maria Helena Bittencourt
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/18391
Resumo: 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.
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spelling The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus Systemic Lupus ErythematosusApoptosisFas proteinBcl-2 proteinC1q complement component 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. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2010-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/1839110.1590/S1807-59322010000300014Clinics; Vol. 65 No. 3 (2010); 327-333 Clinics; v. 65 n. 3 (2010); 327-333 Clinics; Vol. 65 Núm. 3 (2010); 327-333 1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/18391/20454Liphaus, Bernadete L.Kiss, Maria Helena Bittencourtinfo:eu-repo/semantics/openAccess2012-05-23T11:19:44Zoai:revistas.usp.br:article/18391Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2012-05-23T11:19:44Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
title The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
spellingShingle The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
Liphaus, Bernadete L.
Systemic Lupus Erythematosus
Apoptosis
Fas protein
Bcl-2 protein
C1q complement component
title_short The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
title_full The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
title_fullStr The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
title_full_unstemmed The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
title_sort The role of apoptosis proteins and complement components in the etiopathogenesis of systemic lupus erythematosus
author Liphaus, Bernadete L.
author_facet Liphaus, Bernadete L.
Kiss, Maria Helena Bittencourt
author_role author
author2 Kiss, Maria Helena Bittencourt
author2_role author
dc.contributor.author.fl_str_mv Liphaus, Bernadete L.
Kiss, Maria Helena Bittencourt
dc.subject.por.fl_str_mv Systemic Lupus Erythematosus
Apoptosis
Fas protein
Bcl-2 protein
C1q complement component
topic Systemic Lupus Erythematosus
Apoptosis
Fas protein
Bcl-2 protein
C1q complement component
description 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.
publishDate 2010
dc.date.none.fl_str_mv 2010-01-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/18391
10.1590/S1807-59322010000300014
url https://www.revistas.usp.br/clinics/article/view/18391
identifier_str_mv 10.1590/S1807-59322010000300014
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/18391/20454
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 65 No. 3 (2010); 327-333
Clinics; v. 65 n. 3 (2010); 327-333
Clinics; Vol. 65 Núm. 3 (2010); 327-333
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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