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.
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