par Loi, Patrizia 
;Paulart, Frédéric ;Pajak, Bernard ;Nagy, Nathalie ;Salmon, Isabelle ;Moser, Muriel ;Goldman, Michel ;Flamand, Véronique
Référence Transplantation proceedings, 36, 5, page (1275-1279)
Publication Publié, 2004-06
;Paulart, Frédéric ;Pajak, Bernard ;Nagy, Nathalie ;Salmon, Isabelle ;Moser, Muriel ;Goldman, Michel ;Flamand, Véronique Référence Transplantation proceedings, 36, 5, page (1275-1279)
Publication Publié, 2004-06
Article révisé par les pairs
| Résumé : | Ischemia/reperfusion during liver transplantation triggers a complex cascade of inflammatory events that may lead to organ dysfunction. Herein, we investigated the consequences of hepatic ischemia/reperfusion on liver dendritic cells. Liver damage was documented by increased levels of serum alanine aminotransferase and by histopathology showing large areas of hepatocyte cytolysis. MHC class II+ CD45-B220 F4/80 dendritic cells were detected in necrotic areas 20 hours after reperfusion. Dendritic cells freshly isolated from reperfused livers displayed a mature phenotype characterized by upregulated expression of B7 costimulatory molecules; MHC-class II, and CD1d molecules. As shown by real-time PCR, IL-10, and TGF-beta mRNA accumulated in liver dendritic cells isolated after reperfusion, whereas IL-12p40 mRNA levels were decreased and IFN-gamma mRNA levels were unchanged. These results suggest that hepatic ischemia/reperfusion results in maturation of dendritic cells, which preferentially produce inhibitory cytokines. |
