Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Arquivos de Endocrinologia e Metabolismo (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972015000100004 |
Resumo: | Type 1 diabetes mellitus (T1DM) is a chronic, progressive autoimmune disease characterized by metabolic decompensation often leading to dehydration and ketoacidosis. Viral agents seem to play an important role in triggering the autoimmune destruction that leads to the development of T1DM. Among several viral strains investigated so far, the enterovirus family has been consistently associated with the onset of T1DM in humans. One of the mediators of viral damage is the double-stranded RNA (dsRNA) generated during replication and transcription of viral RNA and DNA. The Toll-like receptor 3 (TLR3) gene codes for an endoplasmic receptor of the pattern-recognition receptors (PRRs) family that recognizes dsRNA, plays an important role in the innate immune response triggered by viral infection. Binding of dsRNA to the TLR3 triggers the release of proinflammatory cytokines, such as interferons, which exhibit potent antiviral action; thus, protecting uninfected cells and inducing apoptosis of infected ones. Therefore, the TLR3 gene is a good candidate for the development of T1DM. Within this context, the objective of the present review was to address the role of the TLR3 gene in the development of T1DM. Arch Endocrinol Metab. 2015;59(1):4-12 |
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Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitusAutoimmunitytype 1 diabetes mellitusviral infectionToll-like receptor-3 (TLR3)Type 1 diabetes mellitus (T1DM) is a chronic, progressive autoimmune disease characterized by metabolic decompensation often leading to dehydration and ketoacidosis. Viral agents seem to play an important role in triggering the autoimmune destruction that leads to the development of T1DM. Among several viral strains investigated so far, the enterovirus family has been consistently associated with the onset of T1DM in humans. One of the mediators of viral damage is the double-stranded RNA (dsRNA) generated during replication and transcription of viral RNA and DNA. The Toll-like receptor 3 (TLR3) gene codes for an endoplasmic receptor of the pattern-recognition receptors (PRRs) family that recognizes dsRNA, plays an important role in the innate immune response triggered by viral infection. Binding of dsRNA to the TLR3 triggers the release of proinflammatory cytokines, such as interferons, which exhibit potent antiviral action; thus, protecting uninfected cells and inducing apoptosis of infected ones. Therefore, the TLR3 gene is a good candidate for the development of T1DM. Within this context, the objective of the present review was to address the role of the TLR3 gene in the development of T1DM. Arch Endocrinol Metab. 2015;59(1):4-12Sociedade Brasileira de Endocrinologia e Metabologia2015-02-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972015000100004Archives of Endocrinology and Metabolism v.59 n.1 2015reponame:Arquivos de Endocrinologia e Metabolismo (Online)instname:Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)instacron:SBEM10.1590/2359-3997000000003info:eu-repo/semantics/openAccessAssmann,Taís SilveiraBrondani,Letícia de AlmeidaBouças,Ana PaulaCanani,Luís HenriqueCrispim,Daisyeng2015-07-02T00:00:00Zoai:scielo:S2359-39972015000100004Revistahttps://www.aem-sbem.com/https://old.scielo.br/oai/scielo-oai.php||aem.editorial.office@endocrino.org.br2359-42922359-3997opendoar:2015-07-02T00:00Arquivos de Endocrinologia e Metabolismo (Online) - Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)false |
dc.title.none.fl_str_mv |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
title |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
spellingShingle |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus Assmann,Taís Silveira Autoimmunity type 1 diabetes mellitus viral infection Toll-like receptor-3 (TLR3) |
title_short |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
title_full |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
title_fullStr |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
title_full_unstemmed |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
title_sort |
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus |
author |
Assmann,Taís Silveira |
author_facet |
Assmann,Taís Silveira Brondani,Letícia de Almeida Bouças,Ana Paula Canani,Luís Henrique Crispim,Daisy |
author_role |
author |
author2 |
Brondani,Letícia de Almeida Bouças,Ana Paula Canani,Luís Henrique Crispim,Daisy |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Assmann,Taís Silveira Brondani,Letícia de Almeida Bouças,Ana Paula Canani,Luís Henrique Crispim,Daisy |
dc.subject.por.fl_str_mv |
Autoimmunity type 1 diabetes mellitus viral infection Toll-like receptor-3 (TLR3) |
topic |
Autoimmunity type 1 diabetes mellitus viral infection Toll-like receptor-3 (TLR3) |
description |
Type 1 diabetes mellitus (T1DM) is a chronic, progressive autoimmune disease characterized by metabolic decompensation often leading to dehydration and ketoacidosis. Viral agents seem to play an important role in triggering the autoimmune destruction that leads to the development of T1DM. Among several viral strains investigated so far, the enterovirus family has been consistently associated with the onset of T1DM in humans. One of the mediators of viral damage is the double-stranded RNA (dsRNA) generated during replication and transcription of viral RNA and DNA. The Toll-like receptor 3 (TLR3) gene codes for an endoplasmic receptor of the pattern-recognition receptors (PRRs) family that recognizes dsRNA, plays an important role in the innate immune response triggered by viral infection. Binding of dsRNA to the TLR3 triggers the release of proinflammatory cytokines, such as interferons, which exhibit potent antiviral action; thus, protecting uninfected cells and inducing apoptosis of infected ones. Therefore, the TLR3 gene is a good candidate for the development of T1DM. Within this context, the objective of the present review was to address the role of the TLR3 gene in the development of T1DM. Arch Endocrinol Metab. 2015;59(1):4-12 |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-02-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972015000100004 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972015000100004 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/2359-3997000000003 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Endocrinologia e Metabologia |
publisher.none.fl_str_mv |
Sociedade Brasileira de Endocrinologia e Metabologia |
dc.source.none.fl_str_mv |
Archives of Endocrinology and Metabolism v.59 n.1 2015 reponame:Arquivos de Endocrinologia e Metabolismo (Online) instname:Sociedade Brasileira de Endocrinologia e Metabologia (SBEM) instacron:SBEM |
instname_str |
Sociedade Brasileira de Endocrinologia e Metabologia (SBEM) |
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SBEM |
institution |
SBEM |
reponame_str |
Arquivos de Endocrinologia e Metabolismo (Online) |
collection |
Arquivos de Endocrinologia e Metabolismo (Online) |
repository.name.fl_str_mv |
Arquivos de Endocrinologia e Metabolismo (Online) - Sociedade Brasileira de Endocrinologia e Metabologia (SBEM) |
repository.mail.fl_str_mv |
||aem.editorial.office@endocrino.org.br |
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