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D. , notre groupe a démontré un important défaut de régénération hépatique l'HA, d'explorer les mécanismes physiopathologiques impliqués dans l'interaction du PNN et de l'hépatocyte, et d'évaluer la capacité migratoire des PNN

, Nos travaux ont aussi permis d'identifier la voie NOD1 comme acteur principal dans l'interaction PNN/hépatocytes par le biais de l'expression de molécules d'adhésion. Nos résultats suggèrent cette voie comme cible thérapeutique pour limiter les lésions hépatiques induite par le PNN. De plus, au cours de l'HA, une dérégulation de la voie IL33/sST2 était impliquée dans la migration des PNN. Nous avons démontré une diminution de la capacité migratoire des PNN circulant au cours de l'HA. Le traitement des PNN par l'IL33 était capable de compenser ce défaut migratoire, Notre étude a mis en évidence la voie Hippo/YAP comme étant profondément altérée dans l'HA. L'activation de l'effecteur YAP était anormalement induite dans les hépatocytes de l'HA

. Mots-clés, Hépatite alcoolique, inflammation, PNN, NOD1, IL33/sST2, régénération, Hippo/YAP, et dédifférenciation