Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide
Identifieur interne : 001B19 ( Main/Exploration ); précédent : 001B18; suivant : 001B20Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide
Auteurs : Roberto Lande ; Josh Gregorio ; Valeria Facchinetti ; Bithi Chatterjee [États-Unis] ; Yi-Hong Wang ; Bernhard Homey [Allemagne] ; Wei Cao ; Yui-Hsi Wang ; Bing Su ; Frank O. Nestle [Royaume-Uni] ; Tomasz Zal ; Ira Mellman [États-Unis] ; Jens-Michael Schröder [Allemagne] ; Yong-Jun Liu ; Michel Gilliet [États-Unis]Source :
- Nature [ 0028-0836 ] ; 2007-10-04.
Abstract
Plasmacytoid dendritic cells (pDCs) sense viral and microbial DNA through endosomal Toll-like receptors to produce type 1 interferons. pDCs do not normally respond to self-DNA, but this restriction seems to break down in human autoimmune disease by an as yet poorly understood mechanism. Here we identify the antimicrobial peptide LL37 (also known as CAMP) as the key factor that mediates pDC activation in psoriasis, a common autoimmune disease of the skin. LL37 converts inert self-DNA into a potent trigger of interferon production by binding the DNA to form aggregated and condensed structures that are delivered to and retained within early endocytic compartments in pDCs to trigger Toll-like receptor 9. Thus, our data uncover a fundamental role of an endogenous antimicrobial peptide in breaking innate tolerance to self-DNA and suggest that this pathway may drive autoimmunity in psoriasis.
Url:
DOI: 10.1038/nature06116
Affiliations:
- Allemagne, Royaume-Uni, États-Unis
- District de Düsseldorf, Rhénanie-du-Nord-Westphalie, Schleswig-Holstein
- Düsseldorf, Kiel
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D. Anderson Cancer Center, University of Texas, Houston, Texas 77030</wicri:regionArea><wicri:noRegion>Texas 77030</wicri:noRegion></affiliation><affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Nature</title><idno type="ISSN">0028-0836</idno><idno type="eISSN">1476-4687</idno><imprint><publisher>Nature Publishing Group</publisher><date when="2007-10-04">2007-10-04</date><biblScope unit="vol">449</biblScope><biblScope unit="issue">7162</biblScope><biblScope unit="page" from="564">564</biblScope><biblScope unit="page" to="569">569</biblScope><date type="Copyright" when="2007">2007</date></imprint><idno type="ISSN">0028-0836</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0028-0836</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Plasmacytoid dendritic cells (pDCs) sense viral and microbial DNA through endosomal Toll-like receptors to produce type 1 interferons. pDCs do not normally respond to self-DNA, but this restriction seems to break down in human autoimmune disease by an as yet poorly understood mechanism. Here we identify the antimicrobial peptide LL37 (also known as CAMP) as the key factor that mediates pDC activation in psoriasis, a common autoimmune disease of the skin. LL37 converts inert self-DNA into a potent trigger of interferon production by binding the DNA to form aggregated and condensed structures that are delivered to and retained within early endocytic compartments in pDCs to trigger Toll-like receptor 9. Thus, our data uncover a fundamental role of an endogenous antimicrobial peptide in breaking innate tolerance to self-DNA and suggest that this pathway may drive autoimmunity in psoriasis.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>District de Düsseldorf</li><li>Rhénanie-du-Nord-Westphalie</li><li>Schleswig-Holstein</li></region><settlement><li>Düsseldorf</li><li>Kiel</li></settlement></list><tree><noCountry><name sortKey="Cao, Wei" sort="Cao, Wei" uniqKey="Cao W" first="Wei" last="Cao">Wei Cao</name><name sortKey="Facchinetti, Valeria" sort="Facchinetti, Valeria" uniqKey="Facchinetti V" first="Valeria" last="Facchinetti">Valeria Facchinetti</name><name sortKey="Gregorio, Josh" sort="Gregorio, Josh" uniqKey="Gregorio J" first="Josh" last="Gregorio">Josh Gregorio</name><name sortKey="Lande, Roberto" sort="Lande, Roberto" uniqKey="Lande R" first="Roberto" last="Lande">Roberto Lande</name><name sortKey="Liu, Yong Jun" sort="Liu, Yong Jun" uniqKey="Liu Y" first="Yong-Jun" last="Liu">Yong-Jun Liu</name><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name><name sortKey="Wang, Yi Hong" sort="Wang, Yi Hong" uniqKey="Wang Y" first="Yi-Hong" last="Wang">Yi-Hong Wang</name><name sortKey="Wang, Yui Hsi" sort="Wang, Yui Hsi" uniqKey="Wang Y" first="Yui-Hsi" last="Wang">Yui-Hsi Wang</name><name sortKey="Zal, Tomasz" sort="Zal, Tomasz" uniqKey="Zal T" first="Tomasz" last="Zal">Tomasz Zal</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Chatterjee, Bithi" sort="Chatterjee, Bithi" uniqKey="Chatterjee B" first="Bithi" last="Chatterjee">Bithi Chatterjee</name></noRegion><name sortKey="Chatterjee, Bithi" sort="Chatterjee, Bithi" uniqKey="Chatterjee B" first="Bithi" last="Chatterjee">Bithi Chatterjee</name><name sortKey="Gilliet, Michel" sort="Gilliet, Michel" uniqKey="Gilliet M" first="Michel" last="Gilliet">Michel Gilliet</name><name sortKey="Mellman, Ira" sort="Mellman, Ira" uniqKey="Mellman I" first="Ira" last="Mellman">Ira Mellman</name><name sortKey="Mellman, Ira" sort="Mellman, Ira" uniqKey="Mellman I" first="Ira" last="Mellman">Ira Mellman</name></country><country name="Allemagne"><region name="Rhénanie-du-Nord-Westphalie"><name sortKey="Homey, Bernhard" sort="Homey, Bernhard" uniqKey="Homey B" first="Bernhard" last="Homey">Bernhard Homey</name></region><name sortKey="Schroder, Jens Michael" sort="Schroder, Jens Michael" uniqKey="Schroder J" first="Jens-Michael" last="Schröder">Jens-Michael Schröder</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Nestle, Frank O" sort="Nestle, Frank O" uniqKey="Nestle F" first="Frank O." last="Nestle">Frank O. 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