Chemokines and their receptors in human clinical solid organ transplantation

Abstract

Chemokines and chemokine receptors are expressed in solid organ allografts after ischemia reperfusion injury, acute and chronic rejection and in association with viral infections. The importance of the biology of chemokines and their receptors has been established in several animal models and in humans. Here we discuss evidence for a role for chemokine–chemokine receptor interactions in many posttransplant inflammatory processes. Most compelling are findings that some inducible chemokine receptors are functional in the process of allograft rejection. We discuss evidence that CCR1, CCR5, and CXCR3, interacting with their chemokine ligands—regulation on activation, normal T cell expressed and secreted (RANTES); interferon-inducible protein 10 (IP-10); and monokine induced by interferon-γ (Mig)–are of significance in human allograft rejection. These molecules are functional in rejection, but they may also serve as sensitive diagnostic markers and predictors of patients at risk of rejection or other forms of clinical graft dysfunction. Chemokine receptors warrant consideration as potential therapeutic targets in the future.