Nucleic acid‐sensing TLRs and autoimmunity: novel insights from structural and cell biology
Identifieur interne : 000C80 ( Istex/Corpus ); précédent : 000C79; suivant : 000C81Nucleic acid‐sensing TLRs and autoimmunity: novel insights from structural and cell biology
Auteurs : Karin Pelka ; Takuma Shibata ; Kensuke Miyake ; Eicke LatzSource :
- Immunological Reviews [ 0105-2896 ] ; 2016-01.
Abstract
Invasion of pathogenic microorganisms or tissue damage activates innate immune signaling receptors that sample subcellular locations for foreign molecular structures, altered host molecules, or signs of compartment breaches. Upon engagement of innate immune receptors an acute but transient inflammatory response is initiated, aimed at the clearance of pathogens and cellular debris. Among the molecules that are sensed are nucleic acids, which activate several members of the transmembrane Toll‐like receptor (TLR) family. Inappropriate recognition of nucleic acids by TLRs can cause inflammatory pathologies and autoimmunity. Here, we review the mechanisms involved in triggering nucleic acid‐sensing TLRs and indicate checkpoints that restrict their activation to endolysosomal compartments. These mechanisms are crucial to sample the content of endosomes for nucleic acids in the context of infection or tissue damage, yet prevent accidental activation by host nucleic acids under physiological conditions. Decoding the molecular mechanisms that regulate nucleic acid recognition by TLRs is central to understand pathologies linked to unrestricted nucleic acid sensing and to develop novel therapeutic strategies.
Url:
DOI: 10.1111/imr.12375
Links to Exploration step
ISTEX:17D5D6C35BC84275BC27DDC4C5ED1578FBC925E3Le document en format XML
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Here, we review the mechanisms involved in triggering nucleic acid‐sensing <hi rend="fc">TLR</hi>s and indicate checkpoints that restrict their activation to endolysosomal compartments. These mechanisms are crucial to sample the content of endosomes for nucleic acids in the context of infection or tissue damage, yet prevent accidental activation by host nucleic acids under physiological conditions. Decoding the molecular mechanisms that regulate nucleic acid recognition by <hi rend="fc">TLR</hi>s is central to understand pathologies linked to unrestricted nucleic acid sensing and to develop novel therapeutic strategies.</p></abstract><textClass><keywords><term xml:id="imr12375-kwd-0001"><hi rend="fc">TLR</hi></term><term xml:id="imr12375-kwd-0002">autoimmunity</term><term xml:id="imr12375-kwd-0003"><hi rend="fc">UNC</hi>93B1</term><term xml:id="imr12375-kwd-0004">nucleic acid sensing</term></keywords><keywords rend="articleCategory"><term>Invited Review</term></keywords><keywords rend="tocHeading1"><term>Invited Reviews</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-W8WFSPMD-H/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="imr12375" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-065X</doi><issn type="print">0105-2896</issn><issn type="electronic">1600-065X</issn><idGroup><id type="product" value="IMR"></id></idGroup><titleGroup><title sort="IMMUNOLOGICAL REVIEWS" type="main">Immunological Reviews</title><title type="short">Immunol Rev</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley">10.1111/imr.2016.269.issue-1</doi><titleGroup><title type="specialIssueTitle">Autoimmunity</title></titleGroup><copyright ownership="publisher">© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</copyright><numberingGroup><numbering number="269" type="journalVolume">269</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2016-01">January 2016</coverDate></publicationMeta><publicationMeta level="unit" position="80" status="forIssue" type="reviewArticle"><doi>10.1111/imr.12375</doi><idGroup><id type="unit" value="IMR12375"></id></idGroup><countGroup><count number="16" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Invited Review</title><title type="tocHeading1">Invited Reviews</title></titleGroup><copyright ownership="publisher">© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</copyright><eventGroup><event agent="SPS" date="2015-09-30" type="xmlCreated"></event><event type="firstOnline" date="2015-12-19"></event><event type="publishedOnlineFinalForm" date="2015-12-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:5.0.6 mode:FullText" date="2017-02-10"></event></eventGroup><numberingGroup><numbering type="pageFirst">60</numbering><numbering type="pageLast">75</numbering></numberingGroup><correspondenceTo><lineatedText><line>Correspondence to:</line><line><i>Eicke Latz</i></line><line>Institute of Innate Immunity</line><line>University Hospitals Bonn</line><line>Sigmund‐Freud‐Str. 25</line><line>53127 Bonn, Germany</line><line>Tel.: +49 228 287 51223</line><line>e‐mail: <email>eicke.latz@uni-bonn.de</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:IMR.IMR12375.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Nucleic acid‐sensing <fc>TLR</fc>s and autoimmunity: novel insights from structural and cell biology</title><title type="shortAuthors">Pelka et al</title></titleGroup><creators><creator affiliationRef="#imr12375-aff-0001" creatorRole="author" xml:id="imr12375-cr-0001"><personName><givenNames>Karin</givenNames> <familyName>Pelka</familyName></personName></creator><creator affiliationRef="#imr12375-aff-0002 #imr12375-aff-0003" creatorRole="author" xml:id="imr12375-cr-0002"><personName><givenNames>Takuma</givenNames> <familyName>Shibata</familyName></personName></creator><creator affiliationRef="#imr12375-aff-0002" creatorRole="author" xml:id="imr12375-cr-0003"><personName><givenNames>Kensuke</givenNames> <familyName>Miyake</familyName></personName></creator><creator affiliationRef="#imr12375-aff-0001 #imr12375-aff-0004 #imr12375-aff-0005" corresponding="yes" creatorRole="author" xml:id="imr12375-cr-0004"><personName><givenNames>Eicke</givenNames> <familyName>Latz</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="DE" type="organization" xml:id="imr12375-aff-0001"><orgDiv>Institute of Innate Immunity</orgDiv> <orgName>University Hospitals Bonn</orgName> <address><city>Bonn</city> <country>Germany</country></address></affiliation><affiliation countryCode="JP" type="organization" xml:id="imr12375-aff-0002"><orgDiv>Department of Microbiology and Immunology</orgDiv> <orgDiv>Institute of Medical Science</orgDiv> <orgName>University of Tokyo</orgName> <address><city>Tokyo</city> <country>Japan</country></address></affiliation><affiliation countryCode="JP" type="organization" xml:id="imr12375-aff-0003"><orgDiv>Core Research for Evolutional Science and Technology (CREST)</orgDiv> <orgName>Japan Science and Technology Agency (JST)</orgName> <address><city>Tokyo</city> <country>Japan</country></address></affiliation><affiliation countryCode="DE" type="organization" xml:id="imr12375-aff-0004"><orgName>German Center for Neurodegenerative Diseases</orgName> <address><city>Bonn</city> <country>Germany</country></address></affiliation><affiliation countryCode="US" type="organization" xml:id="imr12375-aff-0005"><orgDiv>Department of Medicine</orgDiv> <orgName>University of Massachusetts Medical School</orgName> <address><city>Worcester</city> <countryPart>MA</countryPart> <country>USA</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="imr12375-kwd-0001"><fc>TLR</fc></keyword><keyword xml:id="imr12375-kwd-0002">autoimmunity</keyword><keyword xml:id="imr12375-kwd-0003"><fc>UNC</fc>93B1</keyword><keyword xml:id="imr12375-kwd-0004">nucleic acid sensing</keyword></keywordGroup><fundingInfo><fundingAgency fundRefName="National Institutes of Health" funderDoi="10.13039/100000002">National Institute of Health (NIH)</fundingAgency></fundingInfo><fundingInfo><fundingAgency fundRefName="Deutsche Forschungsgemeinschaft" funderDoi="10.13039/501100001659">German Research Foundation (DFG)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Excellence Cluster ImmunoSensation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:id="imr12375-abs-0001"><title type="main">Summary</title><p>Invasion of pathogenic microorganisms or tissue damage activates innate immune signaling receptors that sample subcellular locations for foreign molecular structures, altered host molecules, or signs of compartment breaches. Upon engagement of innate immune receptors an acute but transient inflammatory response is initiated, aimed at the clearance of pathogens and cellular debris. Among the molecules that are sensed are nucleic acids, which activate several members of the transmembrane Toll‐like receptor (<fc>TLR</fc>) family. Inappropriate recognition of nucleic acids by <fc>TLR</fc>s can cause inflammatory pathologies and autoimmunity. Here, we review the mechanisms involved in triggering nucleic acid‐sensing <fc>TLR</fc>s and indicate checkpoints that restrict their activation to endolysosomal compartments. These mechanisms are crucial to sample the content of endosomes for nucleic acids in the context of infection or tissue damage, yet prevent accidental activation by host nucleic acids under physiological conditions. Decoding the molecular mechanisms that regulate nucleic acid recognition by <fc>TLR</fc>s is central to understand pathologies linked to unrestricted nucleic acid sensing and to develop novel therapeutic strategies.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Nucleic acid‐sensing TLRs and autoimmunity: novel insights from structural and cell biology</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Nucleic acid‐sensing TLRs and autoimmunity: novel insights from structural and cell biology</title></titleInfo><name type="personal"><namePart type="given">Karin</namePart><namePart type="family">Pelka</namePart><affiliation>Institute of Innate Immunity, University Hospitals Bonn, Bonn, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takuma</namePart><namePart type="family">Shibata</namePart><affiliation>Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan</affiliation><affiliation>Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kensuke</namePart><namePart type="family">Miyake</namePart><affiliation>Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eicke</namePart><namePart type="family">Latz</namePart><affiliation>Institute of Innate Immunity, University Hospitals Bonn, Bonn, Germany</affiliation><affiliation>German Center for Neurodegenerative Diseases, Bonn, Germany</affiliation><affiliation>Department of Medicine, University of Massachusetts Medical School, MA, Worcester, USA</affiliation><affiliation>Correspondence to:Institute of Innate ImmunityUniversity Hospitals BonnSigmund‐Freud‐Str. 2553127 Bonn, GermanyTel.: +49 228 287 51223e‐mail:</affiliation><affiliation>E-mail: eicke.latz@uni-bonn.de</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2016-01</dateIssued><dateCreated encoding="w3cdtf">2015-09-30</dateCreated><copyrightDate encoding="w3cdtf">2016</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Invasion of pathogenic microorganisms or tissue damage activates innate immune signaling receptors that sample subcellular locations for foreign molecular structures, altered host molecules, or signs of compartment breaches. Upon engagement of innate immune receptors an acute but transient inflammatory response is initiated, aimed at the clearance of pathogens and cellular debris. Among the molecules that are sensed are nucleic acids, which activate several members of the transmembrane Toll‐like receptor (TLR) family. Inappropriate recognition of nucleic acids by TLRs can cause inflammatory pathologies and autoimmunity. Here, we review the mechanisms involved in triggering nucleic acid‐sensing TLRs and indicate checkpoints that restrict their activation to endolysosomal compartments. These mechanisms are crucial to sample the content of endosomes for nucleic acids in the context of infection or tissue damage, yet prevent accidental activation by host nucleic acids under physiological conditions. Decoding the molecular mechanisms that regulate nucleic acid recognition by TLRs is central to understand pathologies linked to unrestricted nucleic acid sensing and to develop novel therapeutic strategies.</abstract><note type="funding">National Institute of Health (NIH)</note><note type="funding">German Research Foundation (DFG)</note><note type="funding">Excellence Cluster ImmunoSensation</note><subject><genre>keywords</genre><topic>TLR</topic><topic>autoimmunity</topic><topic>UNC93B1</topic><topic>nucleic acid sensing</topic></subject><relatedItem type="host"><titleInfo><title>Immunological Reviews</title></titleInfo><titleInfo type="abbreviated"><title>Immunol Rev</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Invited Review</topic><topic>Invited Reviews</topic></subject><identifier type="ISSN">0105-2896</identifier><identifier type="eISSN">1600-065X</identifier><identifier type="DOI">10.1111/(ISSN)1600-065X</identifier><identifier type="PublisherID">IMR</identifier><part><date>2016</date><detail type="title"><title>Autoimmunity</title></detail><detail type="volume"><caption>vol.</caption><number>269</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>60</start><end>75</end><total>16</total></extent></part></relatedItem><relatedItem type="references" displayLabel="imr12375-cit-0001"><titleInfo><title>Approaching the asymptote? 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