XXXX -y signaling and @entity59 inhibition together prevent chronic rejection of MHC Class II-mismatched cardiac grafts.

@entity12097 @entity82 @entity3229 @entity455 @entity59 @entity19 @entity26327 @entity6170
BACKGROUND: Chronic rejection can prevent long-term survival of organ transplants. Although the beneficial effects of @entity12097 ( @entity3229 -y) in reducing graft rejection have been reported, the details of the underlying mechanisms remain unclear, especially in the context of modulating cellular infiltration and preventing @entity455 and @entity82 . METHODS: The therapeutic effects of the @entity3229 -y agonist, @entity6170 , combined with anti- @entity59 are explored in a @entity19 model of MHC Class II-histoincompatible cardiac transplantation. RESULTS: @entity6170 treatment alone marginally increased long-term survival and reduced CD8 T-cell infiltration and @entity455 in the grafts. However, there was no reduction in collagen deposition and interleukin (IL)-4, @entity59 and eosinophil infiltration were increased. Anti- @entity59 antibody treatment alone reduced eosinophil infiltration and collagen deposition, but had no effect on CD8 T-cell infiltration or @entity455 . Combined treatment with anti- @entity59 antibody and @entity6170 prevented graft rejection. Furthermore, @entity6170 treatment increased adiponectin receptor II expression in grafts and on dendritic cells and T cells in vitro. Graft survival correlated with increased expression in grafts of the inhibitory molecule @entity26327 . CONCLUSIONS: The findings obtained increase the knowledge on the mode of action of @entity6170 in promoting the survival of MHC Class II-mismatched cardiac transplants in which the CD8 T cells and eosinophils play key roles. @entity3229 -y signaling combined with @entity59 blockade prevents graft rejection.
