Thi study describes the use of CXCl10 as a biomarker to predict transplant rejection.
Interferon (IFN) γ-induced protein 10kDa (IP-10) or C-X-C motif chemokine 10 (CXCL10) is a small cytokine belonging to the CXC chemokine family. This family of signaling molecules is known to control several biological functions and to also play pivotal roles in disease initiation and progression. By binding to its specific cognate receptor CXCR3, CXCL10 critically regulates chemotaxis during several immune-inflammatory processes. In particular, this chemokine controls chemotaxis during the inflammatory response resulting from allograft rejection after transplantation. Interestingly, a strong association has been described between CXCL10 production, immune response and the fate of the graft following allotransplantation. Enhanced CXCL10 production has been observed in recipients of transplants of different organs. This enhanced production likely comes from either the graft or the immune cells and is correlated with an increase in the concentration of circulating CXCL10. Because CXCL10 can be easily measured in the serum and plasma from a patient, the detection and quantitation of circulating CXCL10 could be used to reveal a transplant recipient's immune status. The purpose of this review is to examine the critical role of CXCL10 in the pathogenesis of allograft rejection following organ transplantation. This important role highlights the potential utilization of CXCL10 not only as a therapeutic target but also as a biomarker to predict the severity of rejection, to monitor the inflammatory status of organ recipients and, hopefully, to fine-tune patient therapy in transplantation.
CXCL10: a candidate biomarker in transplantation
CRESCIOLI, CLARA
2012-01-01
Abstract
Interferon (IFN) γ-induced protein 10kDa (IP-10) or C-X-C motif chemokine 10 (CXCL10) is a small cytokine belonging to the CXC chemokine family. This family of signaling molecules is known to control several biological functions and to also play pivotal roles in disease initiation and progression. By binding to its specific cognate receptor CXCR3, CXCL10 critically regulates chemotaxis during several immune-inflammatory processes. In particular, this chemokine controls chemotaxis during the inflammatory response resulting from allograft rejection after transplantation. Interestingly, a strong association has been described between CXCL10 production, immune response and the fate of the graft following allotransplantation. Enhanced CXCL10 production has been observed in recipients of transplants of different organs. This enhanced production likely comes from either the graft or the immune cells and is correlated with an increase in the concentration of circulating CXCL10. Because CXCL10 can be easily measured in the serum and plasma from a patient, the detection and quantitation of circulating CXCL10 could be used to reveal a transplant recipient's immune status. The purpose of this review is to examine the critical role of CXCL10 in the pathogenesis of allograft rejection following organ transplantation. This important role highlights the potential utilization of CXCL10 not only as a therapeutic target but also as a biomarker to predict the severity of rejection, to monitor the inflammatory status of organ recipients and, hopefully, to fine-tune patient therapy in transplantation.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.