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<title lang=en>Interleukin-27 and IFNγ regulate the expression of CXCL9, CXCL10, and CXCL11 in hepatitis</title>
<creator>Basset, Laetitia</creator>
<creator>Chevalier, Sylvie</creator>
<creator>Danger, Yannic</creator>
<creator>Arshad, Muhammad Imran</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>Gascan, Hugues</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>Laboratoire Interdisciplinaire Carnot de Bourgogne (LICB) ; Université de Bourgogne (UB) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Cytokines : structure, signalisation et prolifération tumorale ; Université d'Angers (UA) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>Institut de Génétique et Développement de Rennes (IGDR) ; Université de Rennes 1 (UR1) - Centre National de la Recherche Scientifique (CNRS) - 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>
<description>International audience</description>
<source>ISSN: 0946-2716</source>
<source>EISSN: 1432-1440</source>
<source>Journal of Molecular Medicine</source>
<publisher>Springer Verlag</publisher>
<identifier>hal-01214006</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01214006</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01214006</source>
<source>Journal of Molecular Medicine, Springer Verlag, 2015, 93 (12), pp.1355-1367. 〈10.1007/s00109-015-1319-6〉</source>
<identifier>DOI : 10.1007/s00109-015-1319-6</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1007/s00109-015-1319-6</relation>
<identifier>PUBMED : 26199110</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26199110</relation>
<language>en</language>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Interleukin-27 (IL-27) belongs to the IL-6/IL-12 family of cytokines, associated with different inflammatory diseases and orchestrates its biological activity via common heterodimeric receptor composed of WSX-1 (IL-27Rα) and gp130. The present study was aimed to investigate the regulation of CXCL9, CXCL10, and CXCL11 chemokines in hepatic cells (human LX-2 cell line derived from normal human stellate cells (HSC), primary human hepatocytes, HSC, and HepG2 cells) and concanavalin A (ConA)-induced liver inflammation. We demonstrated that IL-27, but not IL-6, induced/up-regulated CXCR3 ligand genes (CXCL9, CXCL10, and CXCL11; out of 26 selected genes) in a STAT1-dependent manner in hepatic cells in vitro both at transcript and protein levels. In ConA-induced T cell-mediated hepatic model, we showed that soluble IL-27/IFNγ was elevated following ConA hepatitis in association with increased CXCL9, CXCL10, and CXCL11 expression in the liver. The exogenous IL-27 administration induced CXCR3 ligands in mouse liver at 4 h with any significant effect on recruitment of CXCR3(+) immune cells in the liver. The neutralization of IL-27 during ConA hepatitis differentially modulated (transcript vs protein expression) CXCR3 ligands and IFNγ during ConA-induced hepatitis with down-regulated expression of CXCL9 and CXCL10 at transcript level. The IFNγ, complementary regulated the expression of CXCR3 ligands as their up-regulation during ConA hepatitis, was abolished in IFNγ KO mice. In summary, IL-27 up-regulated the CXCL9, CXCL10, and CXCL11 chemokine expression in hepatic cells. IL-27 regulated CXCR3 ligand expression in IFNγ-dependent manner during acute hepatitis suggesting a complementary role of IL-27 and IFNγ to moderate liver inflammation via regulation of CXCR3 ligands. KEY MESSAGE: IL-27 up-regulated CXCR3 ligand expression in human hepatic cells in vitro. IL-27 up-regulated CXCR3 ligand expression and secretion in ConA hepatitis in vivo. CXCR3 ligand expression was down-regulated by blocking IL-27 or IFNγ deficiency. IL-27 modulated liver injury by regulation of CXCR3 ligands in IFNγ-dependent manner.</description>
<date>2015</date>
</dc>
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