The fate of dendritic cells in a mouse model of liver ischemia/reperfusion injury

• Published in: Transplantation proceedings 2004-06, Vol.36 (5), p.1275-1279
• Main Authors: Loi, P, Paulart, F, Pajak, B, Nagy, N, Salmon, I, Moser, M, Goldman, M, Flamand, V
• Format: Article
• Language: English
• Subjects: Alanine Transaminase - analysis; Animals; Biological and medical sciences; Dendritic Cells - immunology; Female; Histocompatibility Antigens Class II - analysis; Liver - blood supply; Liver, biliary tract, pancreas, portal circulation, spleen; Male; Medical sciences; Mice; Mice, Inbred C57BL; Models, Animal; Necrosis; Reperfusion Injury - immunology; Reperfusion Injury - pathology; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Surgery of the digestive system
• ISSN: 0041-1345; 1873-2623
• DOI: 10.1016/j.transproceed.2004.05.052

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-β mRNA accumulated in liver dendritic cells isolated after reperfusion, whereas IL-12p40 mRNA levels were decreased and IFN-γ mRNA levels were unchanged. These results suggest that hepatic ischemia/reperfusion results in maturation of dendritic cells, which preferentially produce inhibitory cytokines.