Liver grafts from CD39-overexpressing rodents are protected from ischemia reperfusion injury due to reduced numbers of resident CD4+ T cells

• DOI: 10.1002/hep.25985
• Publication Date: 2012-07-24T15:08:41Z
• Authors: Sandra Pommey; Bo Lu; Jennifer McRae; John Stagg; Prue Hill; Evelyn Salvaris; Simon C. Robson; Anthony J.F. d'Apice; Peter J. Cowan; Karen M. Dwyer
• Keywords: Viaspan

Ischemia-reperfusion injury (IRI) is a major limiting event for successful liver transplantation, and CD4+ T cells invariant natural killer (iNKT) have been implicated in promoting IRI. We hypothesized that hepatic overexpression of CD39, an ectonucleotidase with antiinflammatory functions, will protect grafts after prolonged cold ischemia. CD39-transgenic (CD39tg) wildtype (WT) mouse livers were transplanted into WT recipients 18 hours storage pathological analysis was performed 6 transplantation. Serum levels alanine aminotransferase interleukin (IL)-6 significantly reduced CD39tg compared to livers. Furthermore, less severe histopathological demonstrated the grafts. Immune revealed iNKT decreased number untreated mice. This associated peripheral cell lymphopenia due defective thymocyte maturation. To assess relative importance liver-resident mediating following extended preservation mice depleted or genetically deficient used as donors. The absence cells, but not protected from early Conclusion: Hepatic play critical role IRI transplant model. (HEPATOLOGY 2013)