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Targeting Toll-Like Receptors for Treatment of SLE

Toll-like receptors (TLRs) are important innate immune receptors for the identification and clearance of invading pathogens. Twelve TLRs that recognize various conserved components of microorganisms are currently known. Among these, the endosomal TLRs 3, 7/8, and 9 recognize dsRNA, ssRNA, and CpG DN...

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Detalles Bibliográficos
Autores principales: Horton, Christopher G., Pan, Zi-jian, Farris, A. Darise
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945668/
https://www.ncbi.nlm.nih.gov/pubmed/20886024
http://dx.doi.org/10.1155/2010/498980
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author Horton, Christopher G.
Pan, Zi-jian
Farris, A. Darise
author_facet Horton, Christopher G.
Pan, Zi-jian
Farris, A. Darise
author_sort Horton, Christopher G.
collection PubMed
description Toll-like receptors (TLRs) are important innate immune receptors for the identification and clearance of invading pathogens. Twelve TLRs that recognize various conserved components of microorganisms are currently known. Among these, the endosomal TLRs 3, 7/8, and 9 recognize dsRNA, ssRNA, and CpG DNA, respectively. Nucleic acid-sensing TLRs, TLR 7 in particular, have been implicated in systemic lupus erythematosus (SLE) and are thought to exacerbate disease pathology. Activation of these TLRs results in the production of inflammatory cytokines and type I interferon. Genome-wide association studies, single nucleotide polymorphism analyses as well as experimental mouse models have provided evidence of TLR signaling involvement in SLE and other autoimmune diseases. Since activation of these receptor pathways promotes autoimmune phenotypes, inhibitory drugs that target these pathways constitute important new therapeutic strategies for the treatment of systemic autoimmunity.
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spelling pubmed-29456682010-09-30 Targeting Toll-Like Receptors for Treatment of SLE Horton, Christopher G. Pan, Zi-jian Farris, A. Darise Mediators Inflamm Review Article Toll-like receptors (TLRs) are important innate immune receptors for the identification and clearance of invading pathogens. Twelve TLRs that recognize various conserved components of microorganisms are currently known. Among these, the endosomal TLRs 3, 7/8, and 9 recognize dsRNA, ssRNA, and CpG DNA, respectively. Nucleic acid-sensing TLRs, TLR 7 in particular, have been implicated in systemic lupus erythematosus (SLE) and are thought to exacerbate disease pathology. Activation of these TLRs results in the production of inflammatory cytokines and type I interferon. Genome-wide association studies, single nucleotide polymorphism analyses as well as experimental mouse models have provided evidence of TLR signaling involvement in SLE and other autoimmune diseases. Since activation of these receptor pathways promotes autoimmune phenotypes, inhibitory drugs that target these pathways constitute important new therapeutic strategies for the treatment of systemic autoimmunity. Hindawi Publishing Corporation 2010 2010-09-19 /pmc/articles/PMC2945668/ /pubmed/20886024 http://dx.doi.org/10.1155/2010/498980 Text en Copyright © 2010 Christopher G. Horton et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Horton, Christopher G.
Pan, Zi-jian
Farris, A. Darise
Targeting Toll-Like Receptors for Treatment of SLE
title Targeting Toll-Like Receptors for Treatment of SLE
title_full Targeting Toll-Like Receptors for Treatment of SLE
title_fullStr Targeting Toll-Like Receptors for Treatment of SLE
title_full_unstemmed Targeting Toll-Like Receptors for Treatment of SLE
title_short Targeting Toll-Like Receptors for Treatment of SLE
title_sort targeting toll-like receptors for treatment of sle
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945668/
https://www.ncbi.nlm.nih.gov/pubmed/20886024
http://dx.doi.org/10.1155/2010/498980
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