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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4191-4199. Prepublished online as a Blood First Edition Paper on February 8, 2005; DOI 10.1182/blood-2004-12-4726. This Article Full Text (PDF) Supplemental Video All Versions of this Article: 2004-12-4726v1 105/11/4191    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Wysocki, C. A Articles by Serody, J. S Search for Related Content PubMed PubMed Citation Articles by Wysocki, C. A Articles by Serody, J. S Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 13, 2004 Accepted January 28, 2005 Leukocyte migration and graft-versus-host disease Christian A Wysocki, Angela Panoskaltsis-Mortari, Bruce R Blazar, and Jonathan S Serody* Departments of Medicine, Microbiology and Immunology, and the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Department of Pediatrics, Division of Pediatric Bone Marrow Transplantation, and the University of Minnesota Cancer Center, University of Minnesota, Minneapolis, MN, USA * Corresponding author; email: onathan_Serody{at}med.unc.edu. Graft-versus-host disease (GVHD) remains a significant complication of allogeneic bone marrow transplantation (allo-BMT). Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction with host antigen presenting cells (APCs). Recent work from our group and others suggests that activated effector T cells exit lymphoid tissues and traffic to mucosal sites and parenchymal target organs such as the GI tract, liver, lung, and skin where they cause tissue damage. The molecular interactions necessary for effector cell migration during GVHD have become the focus of a growing body of research, as these interactions represent potential therapeutic targets. In this review we will discuss chemokine/chemokine receptor interactions and adhesion molecules that have been shown to play roles in effector cell migration in experimental GVHD models, and discuss a potential model for the role of chemokines during the activation phase of GVHD. 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