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...

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Main Authors: Christopher G. Horton, Zi-jian Pan, A. Darise Farris
Format: Article
Language:English
Published: Wiley 2010-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2010/498980
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author Christopher G. Horton
Zi-jian Pan
A. Darise Farris
author_facet Christopher G. Horton
Zi-jian Pan
A. Darise Farris
author_sort Christopher G. Horton
collection DOAJ
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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institution Kabale University
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publishDate 2010-01-01
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spelling doaj-art-88dfa4310ff3477689bc83b4a15738d62025-02-03T06:08:00ZengWileyMediators of Inflammation0962-93511466-18612010-01-01201010.1155/2010/498980498980Targeting Toll-Like Receptors for Treatment of SLEChristopher G. Horton0Zi-jian Pan1A. Darise Farris2Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USAArthritis and Immunology Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USADepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USAToll-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.http://dx.doi.org/10.1155/2010/498980
spellingShingle Christopher G. Horton
Zi-jian Pan
A. Darise Farris
Targeting Toll-Like Receptors for Treatment of SLE
Mediators of Inflammation
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
url http://dx.doi.org/10.1155/2010/498980
work_keys_str_mv AT christopherghorton targetingtolllikereceptorsfortreatmentofsle
AT zijianpan targetingtolllikereceptorsfortreatmentofsle
AT adarisefarris targetingtolllikereceptorsfortreatmentofsle