Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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




Journal article


Current Opinion in Organ Transplantation

Publication Date





100 - 106