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CXCL10:移植中的候选生物标志物。

CXCL10: a candidate biomarker in transplantation.

机构信息

Excellence Center for Research, Transfer and High Education (DENOthe), University of Florence, 50139 Florence, Italy.

出版信息

Clin Chim Acta. 2012 Sep 8;413(17-18):1364-73. doi: 10.1016/j.cca.2012.02.009. Epub 2012 Feb 16.

DOI:10.1016/j.cca.2012.02.009
PMID:22366165
Abstract

Interferon (IFN) γ-induced protein 10 kDa (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.

摘要

干扰素(IFN)γ诱导蛋白 10 kDa(IP-10)或 C-X-C 基序趋化因子 10(CXCL10)是一种属于 CXC 趋化因子家族的小细胞因子。这类信号分子已知可控制多种生物学功能,并在疾病的起始和进展中发挥关键作用。通过与其特定的同源受体 CXCR3 结合,CXCL10 在几种免疫炎症过程中关键地调节趋化作用。特别是,这种趋化因子控制着同种异体移植后排斥反应引起的炎症反应中的趋化作用。有趣的是,在同种异体移植后,CXCL10 的产生、免疫反应与移植物的命运之间存在很强的相关性。在不同器官移植的受者中观察到 CXCL10 产生增强。这种增强的产生可能来自移植物或免疫细胞,与循环 CXCL10 浓度的增加相关。由于 CXCL10 可以在患者的血清和血浆中轻易地被测量到,因此,循环 CXCL10 的检测和定量可用于揭示移植受者的免疫状态。本综述的目的是探讨 CXCL10 在器官移植后同种异体移植物排斥发病机制中的关键作用。这一重要作用突出了 CXCL10 不仅作为治疗靶点的潜在利用,还可作为预测排斥严重程度、监测器官受者炎症状态的生物标志物,以及希望可以精细调整移植患者的治疗。

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