Schenk Austin D, Rosenblum Joshua M, Fairchild Robert L
NB3-59, Department of Immunology, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Clin Lab Med. 2008 Sep;28(3):441-54, vii. doi: 10.1016/j.cll.2008.07.004.
A key event during T cell-mediated rejection of allografts is the trafficking of donor antigen-primed effector T cells from the lymphoid tissue to the graft. This trafficking is mediated in part by chemokine produced in the graftengaging receptors on the T cells and other graftinfiltrating leukocytes. The presence of specific sets of chemokines and chemokine receptors is detectable in rejecting allografts. In animal models, allograft rejection is delayed when chemokine-chemokine receptor function is absent or antagonized but cellular infiltration and graft survival eventually occur, suggesting that T cells and other leukocytes use several trafficking mechanisms during rejection. The use of chemokines as footprints of rejection may be of considerable value as noninvasive biomarkers in transplantation.
在T细胞介导的同种异体移植物排斥反应中，一个关键事件是供体抗原致敏的效应T细胞从淋巴组织向移植物的迁移。这种迁移部分是由移植物中产生的趋化因子介导的，这些趋化因子与T细胞和其他移植物浸润白细胞上的受体结合。在正在发生排斥反应的同种异体移植物中可检测到特定的趋化因子和趋化因子受体。在动物模型中，当趋化因子-趋化因子受体功能缺失或受到拮抗时，同种异体移植物排斥反应会延迟，但最终仍会发生细胞浸润和移植物存活，这表明T细胞和其他白细胞在排斥反应过程中使用多种迁移机制。将趋化因子用作排斥反应的标记物，作为移植中的非侵入性生物标志物可能具有相当大的价值。
