Endothelial cell chimerism after renal transplantation in a XXXX model.

@entity137 @entity63 @entity39 @entity205 @entity35 @entity130
BACKGROUND: Endothelial chimerism, that is, the replacement of damaged donor endothelium by recipient precursors, has been proposed to reduce the allogeneic stimulus and graft rejection. However, both its mechanism and consequence are poorly understood. In this study, we set up a @entity35 model of renal transplantation to investigate the phenomenon of endothelial chimerism and the relationship among the factors involved in its induction, such as @entity130 , severity of graft rejections, and the role of @entity205 @entity137 . METHODS: Female Lewis @entity35 received renal transplants from male Brown Norway kidneys. Groups were divided according to @entity63 or nonischemia of the donor kidney and @entity205 treatment or nonimmunosuppression. To investigate the endothelial chimerism, an in situ hybridization by an X-chromosome-specific DNA probe was performed. The severity of allograft rejection was scored according to the Banff '97 classification. RESULTS: In grafts without @entity130 or without @entity205 treatment, a low degree of endothelial chimerism was detected, although severe vascular rejection and tissue @entity39 developed. More chimerism was found in recipients receiving an ischemic kidney followed by immunosuppressive treatment, although less severe rejection developed. In recipients receiving an ischemic kidney without @entity205 treatment, the highest degree of endothelial chimerism occurred. CONCLUSIONS: Endothelial chimerism demonstrated in @entity35 after renal transplantation may be caused by endothelial damage induced by vascular rejection or @entity63 . @entity63 had the strongest association with the induction of chimerism, which may function as a synergistic promoter. A low-dose @entity205 treatment was shown to inhibit endothelial replacement.
