The fate of dendritic cells in a mouse model of liver ischemia/reperfusion injury.
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.
Loi
P
P
Institute for Medical Immunology-Laboratory of Experimental Immunology, Universite Libre de Bruxelles, Brussels.
Paulart
F
F
Pajak
B
B
Nagy
N
N
Salmon
I
I
Moser
M
M
Goldman
M
M
Flamand
V
V
D000410:Alanine Transaminase / Q000032:analysis; D000818:Animals; D003713:Dendritic Cells / Q000276:immunology*; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D008099:Liver / Q000098:blood supply; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D009336:Necrosis; D015427:Reperfusion Injury / Q000276:immunology* / Q000473:pathology
D000949:Histocompatibility Antigens Class II; D000410:Alanine Transaminase