In vitrodata point to dendritic cells having a key role in development of immune responses, but in the context of organ transplantation, it could be argued that there is surprisingly little evidence currently available to support the attention these cells receive. A general schema is available from other contexts but often leads to confusion between what is suggested should occur and what is known to occur experimentally. Conceptually, in unmodified recipients, donor dendritic cells migrate from the graft to host lymphoid tissues and stimulate host alloresponses, which can eventually lead to graft destruction. As part of the alloresponse, monocytes migrate back to the graft and upon leaving the vasculature become inflammatory macrophages or differentiate into dendritic cells and perform additional roles in the graft. Alternately, given appropriate immunosuppression or tolerizing therapies, donor dendritic cells may live for decades throughout a recipient's tissues and contribute to host acceptance of an allograft. Each outcome involves dendritic cell activation, differentiation and migration, in large part as a result of chemokine binding to specific receptors on dendritic cell surface membranes. This review summarizes current research into the roles of chemokines in dendritic cell functions during alloresponses, with an eye toward therapeutic applications. It also considers what must be established if dendritic cells are to be considered by clinicians as realistic targets to circumvent rejection responses.