Nucleic Acid Immunity in the Pathogenesis of Cutaneous Lupus Erythematosus
Identifieur interne : 000529 ( Pmc/Checkpoint ); précédent : 000528; suivant : 000530Nucleic Acid Immunity in the Pathogenesis of Cutaneous Lupus Erythematosus
Auteurs : Claudia GüntherSource :
- Frontiers in Immunology [ 1664-3224 ] ; 2019.
Abstract
Cutaneous lupus erythematosus can be a devastating painful and mutilating disease that is associated with an inflammatory response in the skin driven by type I interferon activation. Clearance defects in the extra- and intracellular space lead to an enhanced prevalence of nucleic acids that represent danger signals for the innate immune system. Self nucleic acids can stimulate DNA and RNA sensors that have originally evolved to ensure viral defense. Their activation can induce a type I interferon dominated response in resident skin cells, macrophages and dendritic cells that subsequently progresses to adaptive immune stimulation. The genetic exploration of rare monogenic type I interferon driven diseases helped to identify these pathogenic concepts. Based on a genetic susceptibility lupus patients are more vulnerable to environmental trigger factors such as UV-irradiation that can provoke inflammation with local tissue destruction and eventually systemic disease. Understanding of these pathogenic concepts is a prerequisite for development of targeted therapies.
Url:
DOI: 10.3389/fimmu.2019.01636
PubMed: 31379837
PubMed Central: 6646723
Affiliations:
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PMC:6646723Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Cutaneous lupus erythematosus can be a devastating painful and mutilating disease that is associated with an inflammatory response in the skin driven by type I interferon activation. Clearance defects in the extra- and intracellular space lead to an enhanced prevalence of nucleic acids that represent danger signals for the innate immune system. Self nucleic acids can stimulate DNA and RNA sensors that have originally evolved to ensure viral defense. Their activation can induce a type I interferon dominated response in resident skin cells, macrophages and dendritic cells that subsequently progresses to adaptive immune stimulation. The genetic exploration of rare monogenic type I interferon driven diseases helped to identify these pathogenic concepts. Based on a genetic susceptibility lupus patients are more vulnerable to environmental trigger factors such as UV-irradiation that can provoke inflammation with local tissue destruction and eventually systemic disease. Understanding of these pathogenic concepts is a prerequisite for development of targeted therapies.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Immunol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id>
<journal-title-group><journal-title>Frontiers in Immunology</journal-title>
</journal-title-group>
<issn pub-type="epub">1664-3224</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31379837</article-id>
<article-id pub-id-type="pmc">6646723</article-id>
<article-id pub-id-type="doi">10.3389/fimmu.2019.01636</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Immunology</subject>
<subj-group><subject>Mini Review</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Nucleic Acid Immunity in the Pathogenesis of Cutaneous Lupus Erythematosus</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Günther</surname>
<given-names>Claudia</given-names>
</name>
<xref ref-type="corresp" rid="c001"><sup>*</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/666804/overview"></uri>
</contrib>
</contrib-group>
<aff><institution>Department of Dermatology, University Hospital Carl Gustav Carus, Technical University Dresden</institution>
,<addr-line>Dresden</addr-line>
,<country>Germany</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Ralf J. Ludwig, Universität zu Lübeck, Germany</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Luis Enrique Munoz, University of Erlangen Nuremberg, Germany; Victoria Patricia Werth, University of Pennsylvania, United States</p>
</fn>
<corresp id="c001">*Correspondence: Claudia Günther <email>claudia.guenther@uniklinikum-dresden.de</email>
</corresp>
<fn fn-type="other" id="fn001"><p>This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>16</day>
<month>7</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>10</volume>
<elocation-id>1636</elocation-id>
<history><date date-type="received"><day>29</day>
<month>3</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>01</day>
<month>7</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2019 Günther.</copyright-statement>
<copyright-year>2019</copyright-year>
<copyright-holder>Günther</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p>
</license>
</permissions>
<abstract><p>Cutaneous lupus erythematosus can be a devastating painful and mutilating disease that is associated with an inflammatory response in the skin driven by type I interferon activation. Clearance defects in the extra- and intracellular space lead to an enhanced prevalence of nucleic acids that represent danger signals for the innate immune system. Self nucleic acids can stimulate DNA and RNA sensors that have originally evolved to ensure viral defense. Their activation can induce a type I interferon dominated response in resident skin cells, macrophages and dendritic cells that subsequently progresses to adaptive immune stimulation. The genetic exploration of rare monogenic type I interferon driven diseases helped to identify these pathogenic concepts. Based on a genetic susceptibility lupus patients are more vulnerable to environmental trigger factors such as UV-irradiation that can provoke inflammation with local tissue destruction and eventually systemic disease. Understanding of these pathogenic concepts is a prerequisite for development of targeted therapies.</p>
</abstract>
<kwd-group><kwd>nucleic acid immunity</kwd>
<kwd>cutaneous lupus erythematosus</kwd>
<kwd>innate immunity</kwd>
<kwd>nucleic acid sensors</kwd>
<kwd>type I interferon</kwd>
</kwd-group>
<funding-group><award-group><funding-source id="cn001">Deutsche Forschungsgemeinschaft<named-content content-type="fundref-id">10.13039/501100001659</named-content>
</funding-source>
</award-group>
</funding-group>
<counts><fig-count count="2"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="92"></ref-count>
<page-count count="9"></page-count>
<word-count count="7100"></word-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Gunther, Claudia" sort="Gunther, Claudia" uniqKey="Gunther C" first="Claudia" last="Günther">Claudia Günther</name>
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