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Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments

Autoinflammatory diseases are defined as the loss of self-tolerance in which an inflammatory response to self-antigens occurs, which are a significant global burden. Toll-like receptors are key pattern recognition receptors, which integrate signals leading to the activation of transcription factors...

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Detalles Bibliográficos
Autores principales: Duffy, Laura, O’Reilly, Steven C
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5001654/
https://www.ncbi.nlm.nih.gov/pubmed/27579291
http://dx.doi.org/10.2147/ITT.S89795
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author Duffy, Laura
O’Reilly, Steven C
author_facet Duffy, Laura
O’Reilly, Steven C
author_sort Duffy, Laura
collection PubMed
description Autoinflammatory diseases are defined as the loss of self-tolerance in which an inflammatory response to self-antigens occurs, which are a significant global burden. Toll-like receptors are key pattern recognition receptors, which integrate signals leading to the activation of transcription factors and ultimately proinflammatory cytokines. Recently, it has become apparent that these are at the nexus of autoinflammatory diseases making them viable and attractive drug targets. The aim of this review was to evaluate the role of innate immunity in autoinflammatory conditions alongside the role of negative regulation while suggesting possible therapeutic targets.
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spelling pubmed-50016542016-08-30 Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments Duffy, Laura O’Reilly, Steven C Immunotargets Ther Review Autoinflammatory diseases are defined as the loss of self-tolerance in which an inflammatory response to self-antigens occurs, which are a significant global burden. Toll-like receptors are key pattern recognition receptors, which integrate signals leading to the activation of transcription factors and ultimately proinflammatory cytokines. Recently, it has become apparent that these are at the nexus of autoinflammatory diseases making them viable and attractive drug targets. The aim of this review was to evaluate the role of innate immunity in autoinflammatory conditions alongside the role of negative regulation while suggesting possible therapeutic targets. Dove Medical Press 2016-08-22 /pmc/articles/PMC5001654/ /pubmed/27579291 http://dx.doi.org/10.2147/ITT.S89795 Text en © 2016 Duffy and O’Reilly. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Review
Duffy, Laura
O’Reilly, Steven C
Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
title Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
title_full Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
title_fullStr Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
title_full_unstemmed Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
title_short Toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
title_sort toll-like receptors in the pathogenesis of autoimmune diseases: recent and emerging translational developments
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5001654/
https://www.ncbi.nlm.nih.gov/pubmed/27579291
http://dx.doi.org/10.2147/ITT.S89795
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