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Nephrol Dial Transplant (2002) 17: 1374-1379
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

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

Nicholas G. Inston and Paul Cockwell

Department of Nephrology and Renal Transplantation, Queen Elizabeth Hospital, University Hospital Birmingham NHS Trust, Birmingham, UK

Keywords: acute allograft rejection; chemokines; chemokine receptors; graft survival; renal transplantation

The first 150 words of the full text of this article appear below.

Introduction

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 . . . [Full Text of this Article]

T-cell trafficking

Chemokines and their receptors in human renal transplantation

The biology of CXCR3 and CCR5

Animal models for CXCR3 and CCR5 and their ligands

CXCR3 and CCR5 and their ligands in human renal transplantation

CX3CL1/fractalkine

Other chemokines and their receptors in AAR

Conclusions


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