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<title lang=en>TRAIL but not FasL and TNFα, regulates IL-33 expression in murine hepatocytes during acute hepatitis.</title>
<creator>Arshad, Muhammad Imran</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>L'Helgoualc'H, Annie</creator>
<creator>Rauch, Michel</creator>
<creator>Patrat-Delon, Solène</creator>
<creator>Ezan, Frédéric</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Nabti, Sabrina</creator>
<creator>Lehuen, Agnès</creator>
<creator>Cubero, Francisco Javier</creator>
<creator>Girard, Jean-Philippe</creator>
<creator>Trautwein, Christian</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>Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>Immunité et cancer (U932) ; Université Paris Descartes - Paris 5 (UPD5) - Institut Curie - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Immunologie et génétique du diabète de type 1, génétique multifactorielle en endocrinologie pédiatrique (U986) ; Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Medical Department III ; University Hospital Aachen</contributor>
<contributor>Institut de pharmacologie et de biologie structurale (IPBS) ; Université Paul Sabatier - Toulouse 3 (UPS) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<description>International audience</description>
<source>ISSN: 0270-9139</source>
<source>EISSN: 1527-3350</source>
<source>Hepatology</source>
<publisher>Wiley-Blackwell</publisher>
<identifier>hal-00874194</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00874194</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00874194</source>
<source>Hepatology, Wiley-Blackwell, 2012, 56 (6), pp.2353-62. 〈10.1002/hep.25893〉</source>
<identifier>PUBMED : 22961755</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/22961755</relation>
<identifier>DOI : 10.1002/hep.25893</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1002/hep.25893</relation>
<language>en</language>
<subject>[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>UNLABELLED: Interleukin (IL)-33, a member of the IL-1 cytokine family, positively correlates with acute hepatitis and chronic liver failure in mice and humans. IL-33 is expressed in hepatocytes and is regulated by natural killer T (NKT) cells during concanavalin A (ConA)-induced acute liver injury. Here, we investigated the molecular mechanisms underlying the expression of IL-33 during acute hepatitis. The expression of IL-33 and its regulation by death receptor pathways was investigated after the induction of ConA-acute hepatitis in wildtype (WT), perforin(-/-) , tumor necrosis factor related apoptosis inducing ligand (TRAIL)(-/-) , and NKT cell-deficient (CD1d(-/-) ) mice. In addition, we used a model of acute liver injury by administering Jo2/Fas-antibody or D-galactosamine-tumor necrosis factor alpha (TNFα) in WT mice. Finally, the effect of TRAIL on IL-33 expression was assessed in primary cultured murine hepatocytes. We show that IL-33 expression in hepatocytes is partially controlled by perforin during acute liver injury, but not by TNFα or Fas ligand (FasL). Interestingly, the expression of IL-33 in hepatocytes is blocked during ConA-acute hepatitis in TRAIL-deficient mice compared to WT mice. In contrast, administration of recombinant murine TRAIL associated with ConA-priming in CD1d-deficient mice or in vitro stimulation of murine hepatocytes by TRAIL but not by TNFα or Jo2 induced IL-33 expression in hepatocytes. The IL-33-deficient mice exhibited more severe ConA liver injury than WT controls, suggesting a protective effect of IL-33 in ConA-hepatitis. CONCLUSION: The expression of IL-33 during acute hepatitis is dependent on TRAIL, but not on FasL or TNFα.</description>
<date>2012-12</date>
</dc>
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