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Liver-derived IL-10 as a potential inhibitor of a TH1-deviating crosstalk between donor DC and recipient NK cells during combined liver-kidney transplantation

Conference paper
Authors Madeleine Ingelsten
Karin Gustafsson
Michael Olausson
Börje Haraldsson
Jenny Nyström
Alex Karlsson-Parra
Published in The Transplantation society XI Basic science symposium, European society for organ transplantation I Basic science meeting, Brussels 2009.
Publication year 2009
Published at Institute of Clinical Sciences, Department of Surgery
Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Subject categories Immunobiology, Clinical immunology, Transplantation surgery

Abstract

During transplantation DCs within the allograft become activated and migrate to secondary lymphoid organs (SLO) where they activate NK cells and alloreactive T cell. Previous findings suggest that a liver graft is less prone to induce rejection compared to a renal graft but the mechanisms are still unclear. We compared changes in graft gene expression of inflammatory mediators known to participate in transplantation-induced DC activation in the liver and kidney in patients undergoing combined liver-kidney transplantation (n=8). Real-time PCR analysis revealed a similar up-regulation of mRNA for the DC-activation-associated inflammatory mediators TNF-α, IL-1β and IFN-gamma after reperfusion in the liver and kidney. While no reperfusion-dependent mRNA increase for IL-10 was found in transplated grafts, serial measurement of cytokine levels in peripheral blood revealed that IL-10 levels increased 60-fold in serum shortly (within 1 h) after liver, but before kidney, reperfusion and returned to pre-transplant levels at day 2 post-transplantation (n=3). No significant changes were seen in IL-12 levels. DCs matured with a cocktail consisting of IFN-γ, TNF-α and IL-1β demonstrated a strong and sustained production of CXCR3-ligands which are indispensable for DC-mediated recruitment of blood NK cells into SLO and their subsequent boosting of TH1-deviated alloresponses. Addition of IL-10 during DC maturation significantly decreased the production of all three CXCR3-ligands (CXCL9, CXCL10 and CXCL11). These findings indicate that IL-10 is selectively and rapidly released during liver transplantation, probably due to accumulation during the ischehmia period. This release may potentially inhibit a TH1-deviating crosstalk between donor DC and recipient NK cells.

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