Free HTLV-1 induces TLR7-dependent innate immune response and TRAIL relocalization in killer plasmacytoïd dendritic cells.
Identifieur interne : 000253 ( France/Analysis ); précédent : 000252; suivant : 000254Free HTLV-1 induces TLR7-dependent innate immune response and TRAIL relocalization in killer plasmacytoïd dendritic cells.
Auteurs : R. Colisson [France] ; L. Barblu [France] ; C. Gras [France] ; F. Raynaud [France] ; R. Hadj-Slimane [France] ; C. Pique [France] ; O. Hermine [France] ; Y. Lepelletier [France] ; J. P. Herbeuval [France]Source :
- Blood [ 0006-4971 ] ; 2010.
English descriptors
Abstract
A recent report demonstrated that free human T-cell leukemia virus 1 (HTLV-1) could infect plasmacytoid dendritic cells (pDCs). The major role of pDCs is to secrete massive levels of interferon-alpha (IFN-alpha) upon virus exposure; however, the induction of IFN-alpha by HTLV-1 remains unknown. We demonstrate here that cell-free HTLV-1 generated a pDC innate immune response by producing massive levels of IFN-alpha that were inhibited by anti-HTLV-1 antibodies. HTLV-1 induced costimulatory molecules and rapid expression of the apoptotic ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Furthermore, HTLV-1 stimulated pDC-induced apoptosis of CD4(+) T cells expressing DR5, transforming pDCs into IFN-producing killer pDCs. We also observed that an endosomal acidification inhibitor and a Toll-like receptor-7 (TLR7)-specific blocker drastically inhibited pDC response to HTLV-1. Three-dimensional microscopy analysis revealed that unstimulated pDCs were "dormant" IFN-producing killer pDCs with high levels of intracellular TRAIL that could be rapidly mobilized to the surface in response to TLR7 activation. Inhibition of viral degradation in endosomes by chloroquine maintained viral integrity, allowing virus detection by 3-dimensional microscopy. We demonstrate that pDCs respond to cell-free HTLV-1 by producing high levels of IFN-alpha and by mobilizing TRAIL on cell surface after TLR7 triggering. This is the first demonstration of an innate immune response induced by free HTLV-1.
Url:
DOI: 10.1182/blood-2009-06-224741
Affiliations:
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Hal:hal-00456470Le document en format XML
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<orgName>Institut National de la Santé et de la Recherche Médicale</orgName>
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<desc> <address> <addrLine>101, rue de Tolbiac, 75013 Paris </addrLine>
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<orgName>Centre National de la Recherche Scientifique</orgName>
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<country>France</country>
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<author><name sortKey="Lepelletier, Y" sort="Lepelletier, Y" uniqKey="Lepelletier Y" first="Y." last="Lepelletier">Y. Lepelletier</name>
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<orgName>Cytokines, hématopoïèse et réponse immune</orgName>
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<tutelle name="UMR 8147" active="#struct-303623" type="direct"><org type="institution" xml:id="struct-303623" status="VALID"> <idno type="IdRef">026388278</idno>
<orgName>Institut National de la Santé et de la Recherche Médicale</orgName>
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<tutelle name="UMR 8147" active="#struct-441569" type="direct"><org type="institution" xml:id="struct-441569" status="VALID"> <idno type="IdRef">02636817X</idno>
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<orgName>Centre National de la Recherche Scientifique</orgName>
<orgName type="acronym">CNRS</orgName>
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<country>France</country>
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</author>
<author><name sortKey="Herbeuval, J P" sort="Herbeuval, J P" uniqKey="Herbeuval J" first="J. P." last="Herbeuval">J. P. Herbeuval</name>
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<orgName>Cytokines, hématopoïèse et réponse immune</orgName>
<orgName type="acronym">CHRI</orgName>
<date type="start">2004</date>
<date type="end">2014</date>
<desc> <address> <addrLine>Bâtiment Sèvres - Porte I 161 Rue de Sèvres 75743 PARIS CEDEX 15</addrLine>
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<orgName>Université Paris Descartes - Paris 5</orgName>
<orgName type="acronym">UPD5</orgName>
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<tutelle name="UMR 8147" active="#struct-303623" type="direct"><org type="institution" xml:id="struct-303623" status="VALID"> <idno type="IdRef">026388278</idno>
<orgName>Institut National de la Santé et de la Recherche Médicale</orgName>
<orgName type="acronym">INSERM</orgName>
<desc> <address> <addrLine>101, rue de Tolbiac, 75013 Paris </addrLine>
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</address>
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</desc>
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<idno type="ISNI">0000000122597504</idno>
<orgName>Centre National de la Recherche Scientifique</orgName>
<orgName type="acronym">CNRS</orgName>
<date type="start">1939-10-19</date>
<desc> <address> <country key="FR"></country>
</address>
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</hal:affiliation>
<country>France</country>
</affiliation>
</author>
</analytic>
<idno type="DOI">10.1182/blood-2009-06-224741</idno>
<series><title level="j">Blood</title>
<idno type="ISSN">0006-4971</idno>
<imprint><date type="datePub">2010</date>
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<profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>chloroquine</term>
<term>dendritic cells</term>
<term>human t-lymphotropic virus 1</term>
<term>immune response</term>
<term>viruses</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"> <p>A recent report demonstrated that free human T-cell leukemia virus 1 (HTLV-1) could infect plasmacytoid dendritic cells (pDCs). The major role of pDCs is to secrete massive levels of interferon-alpha (IFN-alpha) upon virus exposure; however, the induction of IFN-alpha by HTLV-1 remains unknown. We demonstrate here that cell-free HTLV-1 generated a pDC innate immune response by producing massive levels of IFN-alpha that were inhibited by anti-HTLV-1 antibodies. HTLV-1 induced costimulatory molecules and rapid expression of the apoptotic ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Furthermore, HTLV-1 stimulated pDC-induced apoptosis of CD4(+) T cells expressing DR5, transforming pDCs into IFN-producing killer pDCs. We also observed that an endosomal acidification inhibitor and a Toll-like receptor-7 (TLR7)-specific blocker drastically inhibited pDC response to HTLV-1. Three-dimensional microscopy analysis revealed that unstimulated pDCs were "dormant" IFN-producing killer pDCs with high levels of intracellular TRAIL that could be rapidly mobilized to the surface in response to TLR7 activation. Inhibition of viral degradation in endosomes by chloroquine maintained viral integrity, allowing virus detection by 3-dimensional microscopy. We demonstrate that pDCs respond to cell-free HTLV-1 by producing high levels of IFN-alpha and by mobilizing TRAIL on cell surface after TLR7 triggering. This is the first demonstration of an innate immune response induced by free HTLV-1.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
</country>
</list>
<tree><country name="France"><noRegion><name sortKey="Colisson, R" sort="Colisson, R" uniqKey="Colisson R" first="R." last="Colisson">R. Colisson</name>
</noRegion>
<name sortKey="Barblu, L" sort="Barblu, L" uniqKey="Barblu L" first="L." last="Barblu">L. Barblu</name>
<name sortKey="Gras, C" sort="Gras, C" uniqKey="Gras C" first="C." last="Gras">C. Gras</name>
<name sortKey="Hadj Slimane, R" sort="Hadj Slimane, R" uniqKey="Hadj Slimane R" first="R." last="Hadj-Slimane">R. Hadj-Slimane</name>
<name sortKey="Herbeuval, J P" sort="Herbeuval, J P" uniqKey="Herbeuval J" first="J. P." last="Herbeuval">J. P. Herbeuval</name>
<name sortKey="Hermine, O" sort="Hermine, O" uniqKey="Hermine O" first="O." last="Hermine">O. Hermine</name>
<name sortKey="Lepelletier, Y" sort="Lepelletier, Y" uniqKey="Lepelletier Y" first="Y." last="Lepelletier">Y. Lepelletier</name>
<name sortKey="Pique, C" sort="Pique, C" uniqKey="Pique C" first="C." last="Pique">C. Pique</name>
<name sortKey="Raynaud, F" sort="Raynaud, F" uniqKey="Raynaud F" first="F." last="Raynaud">F. Raynaud</name>
</country>
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