title: Chemokine-directed strategies to attenuate allograft rejection.
abstract: 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.
authors.affiliation: NB3-59, Department of Immunology, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
authors.forename: Austin D
authors.initials: AD
authors.lastname: Schenk
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Rosenblum
authors.forename: Robert L
authors.initials: RL
authors.lastname: Fairchild
mesh_terms: D000818:Animals; D018925:Chemokines / Q000502:physiology*; D006084:Graft Rejection / Q000276:immunology / Q000517:prevention & control*; D006801:Humans; D051379:Mice; D051381:Rats; D019707:Receptors, Chemokine / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D018925:Chemokines; D019707:Receptors, Chemokine