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Ischemia/reperfusion injury is an unavoidable consequence of organ transplantation that results in the generation of reactive oxygen species and the initiation of an inflammatory response. The characteristic features of ischemia/reperfusion injury involve the activation of endothelium by reactive oxygen species and inflammatory cytokines, induction of adhesion molecules (for example, P-selectin and E-selectin), adherence of platelets, and infiltration by leukocytes consisting initially of neutrophils with subsequent infiltration by monocytes, macrophages, and T lymphocytes. In this review, we consider the current evidence for involvement of chemokines during the period after ischemia/reperfusion injury and examine the temporal relation between chemokine expression and leukocyte infiltration. Changes in the profile of chemokines after ischemia/reperfusion injury, in association with upregulation of endothelial adhesion molecules, may contribute to the immunogenicity of a transplanted organ by increasing its ability to recruit particular leukocyte subsets at specific time points after ischemia/reperfusion injury. © 2002 Lippincott Williams & Wilkins, Inc.

Original publication

DOI

10.1097/00075200-200203000-00019

Type

Journal article

Journal

Current Opinion in Organ Transplantation

Publication Date

01/01/2002

Volume

7

Pages

100 - 106