Abstract

We describe a regulatory lymphoid dendritic cell (LDC) population propagated from mouse liver nonparenchymal cells (NPC) in IL-3 and anti-CD40 monoclonal antibody that are phenotypically mature, and induce T-cell hyporesponsiveness by promoting T-cell apoptotic death, which is partially caspase-dependent, but is unlikely to be mediated by soluble factor(s). In vivo administration of liver LDC significantly prolonged the survival of vascularized cardiac allografts in an alloantigen-specific manner. This is associated with enhanced T-cell death in secondary lymphoid organs.

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