The evolving role of chemokines and their receptors in acute allograft rejection

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Abstract
In renal transplantation, the occurrence of one or more episodes of acute allograft rejection (AAR) is a major determinant of graft survival [1]. Most episodes of AAR are caused by cell‐mediated processes and require the infiltration of alloactivated T cells into the engrafted organ. These cells are characterized by the expression of surface markers indicating a memory (CD45RO+) and/or activated (CD25+) phenotype [2,3], which develop subsequent to T‐cell receptor (TCR) interactions with MHC–alloantigen complexes or donor MHC in secondary lymphoid tissue [4]. A further result of this process is the expression of chemokine receptors that direct the trafficking of alloactivated T cells into the graft in response to local production of chemokines, initially by resident cells. There is now deep interest in this area that reflects the recent identification of restricted chemokine–receptor interactions as key functional events in T‐cell recruitment and potential therapeutic targets for the prophylaxis of AAR. We discuss this recent evidence and how it relates to our current knowledge of chemokine–receptor expression in human renal transplantation.

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