XXXX may modulate dendritic cells activation in kidney transplant recipients with delayed graft function.

@entity650 @entity8 @entity556 @entity1356 @entity310 @entity4897 @entity4417 @entity3646 @entity688 @entity4155 @entity8428 @entity379 @entity2935 @entity8781 @entity2841 @entity12867
BACKGROUND: Coagulation and complement activation represent key events in ischaemia-reperfusion-induced @entity8 leading to delayed graft function (DGF). It is still unclear whether the coagulation cascade may also influence the acquired immunity. The aim of the present study was to investigate the expression of @entity8781 ( @entity8781 ), the main @entity556 receptor, by graft-infiltrating dendritic cells (DCs), and to evaluate whether @entity556 may influence DCs complement production and T-cell response. METHODS: @entity8781 , @entity4897 , @entity2935 , @entity12867 , fibrin, C3c and @entity8428 protein expression were evaluated by confocal microscopy. Cultured DCs were obtained incubating monocytes (Ms) with @entity3646 and @entity2841 . DC maturation was obtained with @entity379 +sCD40L or with a cytokine cocktail ( @entity1356 , @entity310 , PGE2, @entity650 ). @entity8781 protein expression on cultured DC was evaluated by flow-cytometry. Complement receptors, C3, IL12/IL17p40 and @entity688 gene expression was evaluated by qPCR. T cell phenotype was evaluated by ELISPOT. @entity379 protein presence was evaluated by ELISA. RESULTS: @entity8781 was expressed by infiltrating myeloid DCs in pre-transplant and in DGF biopsies. In DGF grafts, myeloid DCs localized within fibrin and @entity8428 deposits and expressed C3c. In vitro, @entity8781 protein expression was increased in monocyte-derived immature DCs and in cytokine-induced mature DCs compared to monocytes. @entity8781 activation caused a time-dependent increase in C3 and complement receptors expression. Moreover, @entity556 stimulation, while reducing @entity688 mRNA abundance, induced interleukin-12/IL-17 p40 gene expression, and promoted @entity4417 ability to increase interleukin-12/ @entity4155 mRNA abundance. These changes in the DCs' cytokine pattern influenced their ability to induce interferon-g production by T cells, suggesting the activation of a T helper-1 bias. CONCLUSION: Our data suggest that @entity8781 is expressed by DCs in DGF grafts and its activation may induce complement production and a Th1 bias. This observation suggests a potential pathogenic link between DGF and acquired allo-response leading to graft damage.
