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<title lang=en>PARP2 deficiency affects invariant-NKT,-cell maturation and protects mice from ,Concanavalin A-induced liver injury.</title>
<creator>Filliol, Aveline</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>Dion, Sarah</creator>
<creator>Genet, Valentine</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Dantzer, Françoise</creator>
<creator>Samson, Michel</creator>
<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>Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC) ; Université de Rennes 1 (UR1) - IFR140</contributor>
<contributor>Génétique, Immunothérapie, Chimie et Cancer (GICC) ; Université François Rabelais - Tours - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>Poly(ADP-ribosyl)ation et Intégrité du Génome ; Université Louis Pasteur - Strasbourg I - Ecole Supérieure de Biotechnologie de Strasbourg - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>We thank the dedicated platforms for immunohistochemistry analysis and animal house facilities (i.e., H2P2 and animal house platforms) of SFR BIOSIT, University of Rennes 1, France.</contributor>
<description>International audience</description>
<source>ISSN: 0193-1857</source>
<source>EISSN: 1522-1547</source>
<source>AJP - Gastrointestinal and Liver Physiology</source>
<publisher>American Physiological Society</publisher>
<identifier>hal-01630440</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01630440</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01630440/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01630440/file/102513_1_merged_1499199857-1.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01630440</source>
<source>AJP - Gastrointestinal and Liver Physiology, American Physiological Society, 2017, 313 (5), pp.G399-G409. 〈10.1152/ajpgi.00436.2016〉</source>
<identifier>DOI : 10.1152/ajpgi.00436.2016</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpgi.00436.2016</relation>
<identifier>PUBMED : 28751426</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/28751426</relation>
<language>en</language>
<subject lang=en>Parp</subject>
<subject lang=en> autoimmune hepatitis</subject>
<subject lang=en> hepatitis</subject>
<subject lang=en> liver</subject>
<subject lang=en> natural killer T cells</subject>
<subject>[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology</subject>
<subject>[SDV.IMM] Life Sciences [q-bio]/Immunology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Excessive or persistent inflammation and hepatocyte death are the key triggers of liver diseases. The poly(ADP-ribose) polymerase (PARP) proteins induce cell death and inflammation. Chemical inhibition of PARP activity protects against liver injury during concanavalin A (ConA)-induced hepatitis. In this mice model, ConA activates immune cells, which promote inflammation and induce hepatocyte death, mediated by the activated invariant natural killer T (iNKT) lymphocyte population. We analyzed immune cell populations in the liver and several lymphoid organs, such as the spleen, thymus, and bone marrow in Parp2-deficient mice to better define the role of PARP proteins in liver immunity and inflammation at steady state and during ConA-induced hepatitis. We show that 1) the genetic inactivation of Parp2, but not Parp1, protected mice from ConA hepatitis without deregulating cytokine expression and leucocyte recruitment; 2) cellularity was lower in the thymus, but not in spleen, liver, or bone marrow of Parp2-/- mice; 3) spleen and liver iNKT lymphocytes, as well as thymic T and NKT lymphocytes were reduced in Parp2 knockout mice. In conclusion, our results suggest that the defect of T-lymphocyte maturation in Parp2 knockout mice leads to a systemic reduction of iNKT cells, reducing hepatocyte death during ConA-mediated liver damage, thus protecting the mice from hepatitis.NEW & NOTEWORTHY The genetic inactivation of Parp2, but not Parp1, protects mice from concanavalin A hepatitis. Immune cell populations are lower in the thymus, but not in the spleen, liver, or bone marrow of Parp2-deficient mice compared with wild-type mice. Spleen and liver invariant natural killer T (NKT) lymphocytes, as well as thymic T and NKT lymphocytes, are reduced in Parp2-deficient mice</description>
<date>2017</date>
</dc>
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