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<title lang=en>CD95-Mediated Calcium Signaling Promotes T Helper 17 Trafficking to Inflamed Organs in Lupus-Prone Mice</title>
<creator>Poissonnier, Amanda</creator>
<creator>Sanseau, Doriane</creator>
<creator>Le Gallo, Matthieu</creator>
<creator>Malleter, Marine</creator>
<creator>Levoin, Nicolas</creator>
<creator>Viel, Roselyne</creator>
<creator>Morere, Lucie</creator>
<creator>Penna, Aubin</creator>
<creator>Blanco, Patrick</creator>
<creator>Dupuy, Alain</creator>
<creator>Poizeau, Florence</creator>
<creator>Fautrel, Alain</creator>
<creator>Seneschal, Julien</creator>
<creator>Jouan, Florence</creator>
<creator>Ritz, Jerome</creator>
<creator>Forcade, Edouard</creator>
<creator>Rioux, Nathalie</creator>
<creator>Contin-Bordes, Cécile</creator>
<creator>Ducret, Thomas</creator>
<creator>Vacher, Anne-Marie</creator>
<creator>Barrow, Paul A.</creator>
<creator>Flynn, Robin J.</creator>
<creator>Vacher, Pierre</creator>
<creator>Legembre, Patrick</creator>
<contributor>Oncogenesis Stress Signaling (OSS) ; Université de Rennes 1 (UR1) - CRLCC Eugène Marquis (CRLCC)</contributor>
<contributor>CRLCC Eugène Marquis (CRLCC)</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Laboratoire Bioprojet ; Laboratoire Bioprojet</contributor>
<contributor>H2P2 - Histo Pathologie Hight Precision (H2P2) ; Université de Rennes 1 (UR1) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Composantes innées de la réponse immunitaire et différenciation (CIRID) ; Université Bordeaux Segalen - Bordeaux 2 - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>CHU Pontchaillou [Rennes]</contributor>
<contributor>Foie, métabolismes et cancer ; Université de Rennes 1 (UR1) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Biothérapies des maladies génétiques et cancers ; Université Bordeaux Segalen - Bordeaux 2 - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Service d'anatomie et cytologie pathologiques [Rennes] ; Université de Rennes 1 (UR1) - Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>Service d'immunologie et d'immunogénétique [Bordeaux] ; Université Bordeaux Segalen - Bordeaux 2 - CHU Bordeaux [Bordeaux]</contributor>
<contributor>Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB) ; Université Bordeaux Segalen - Bordeaux 2 - CHU Bordeaux [Bordeaux] - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Validation et identification de nouvelles cibles en oncologie (VINCO) ; Université Bordeaux Segalen - Bordeaux 2 - Institut Bergonié - CRLCC Bordeaux - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Université Bordeaux Segalen - Bordeaux 2</contributor>
<contributor>INCa PLBIO</contributor>
<contributor> Ligue Contre le Cancer</contributor>
<contributor> INSERM Transfert</contributor>
<contributor> Fondation ARC</contributor>
<contributor> Region Bretagne</contributor>
<contributor> Rennes Metropole</contributor>
<contributor> University of Nottingham Faculty of Medicine</contributor>
<contributor> Biotechnology and Biological Sciences Research Council [BB/M018369/1]</contributor>
<contributor> ANR [ANR-12-JSV2-0004-001]</contributor>
<description>International audience</description>
<source>ISSN: 1074-7613</source>
<source>Immunity</source>
<publisher>Elsevier</publisher>
<identifier>hal-01359568</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01359568</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01359568</source>
<source>Immunity, Elsevier, 2016, 45 (1), pp.209--223. 〈10.1016/j.immuni.2016.06.028〉</source>
<identifier>DOI : 10.1016/j.immuni.2016.06.028</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.immuni.2016.06.028</relation>
<identifier>PUBMED : 27438772</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/27438772</relation>
<language>en</language>
<subject lang=en>autoimmune lymphoproliferative syndrome</subject>
<subject lang=en> fas gene-mutations</subject>
<subject lang=en> sh3 domain</subject>
<subject lang=en> protein</subject>
<subject lang=en> apoptosis</subject>
<subject lang=en> receptor</subject>
<subject lang=en> cd95</subject>
<subject lang=en> pathway</subject>
<subject lang=en> ligand</subject>
<subject lang=en> death</subject>
<subject>[SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>CD95 ligand (CD95L) is expressed by immune cells and triggers apoptotic death. Metalloprotease-cleaved CD95L (cl-CD95L) is released into the bloodstream but does not trigger apoptotic signaling. Hence, the pathophysiological role of cl-CD95L remains unclear. We observed that skin-derived endothelial cells from systemic lupus erythematosus (SLE) patients expressed CD95L and that after cleavage, cl-CD95L promoted T helper 17 (Th17) lymphocyte transmigration across the endothelial barrier at the expense of T regulatory cells. T cell migration relied on a direct interaction between the CD95 domain called calcium-inducing domain (CID) and the Src homology 3 domain of phospholipase C gamma 1. Th17 cells stimulated with cl-CD95L produced sphingosine-1-phosphate (S1P), which promoted endothelial transmigration by activating the S1P receptor 3. We generated a cell-penetrating CID peptide that prevented Th17 cell transmigration and alleviated clinical symptoms in lupus mice. Therefore, neutralizing the CD95 non-apoptotic signaling pathway could be an attractive therapeutic approach for SLE treatment.</description>
<date>2016</date>
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