Chemokine-directed strategies to attenuate allograft rejection.

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.