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Blood, 1 October 2004, Vol. 104, No. 7, pp. 2187-2193. Prepublished online as a Blood First Edition Paper on June 1, 2004; DOI 10.1182/blood-2004-03-1040. This Article Full Text (PDF) All Versions of this Article: 2004-03-1040v1 104/7/2187    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 Miura, Y. Articles by Hess, A. D Search for Related Content PubMed PubMed Citation Articles by Miura, Y. Articles by Hess, A. D Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 19, 2004 Accepted May 3, 2004 Association of Foxp3 regulatory gene expression with graft-versus-host disease Yuji Miura, Christopher J Thoburn, Emilie C Bright, Michele L Phelps, Tahiro Shin, Elizabeth C Matsui, William H Matsui, Sally Arai, Ephraim J Fuchs, Georgia B Vogelsang, Richard J Jones, and Allan D Hess* The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA Pediatrics, Johns Hopkins University, Baltimore, MD, USA Bone Marrow Transplant and Cell Therapy, Ruth Presbyterian St. Luke's Medical Center, Chicago, IL, USA * Corresponding author; email: adhess{at}jhmi.edu. Graft-versus-host disease (GVHD) is characterized by an impairment of mechanisms that underlie the development of immunological tolerance. While the cytokine storm associated with GVHD leads to expression of cell surface markers on both effector and regulatory T cells, regulatory CD4+ T cells that play an instrumental role in the maintenance of tolerance appear to uniquely express the Foxp3 transcriptional repressor. Foxp3 mRNA expression was significantly decreased in peripheral blood mononuclear cells from patients with either allogeneic GVHD or autologous GVHD compared to patients without GVHD. Expression of Foxp3 negatively correlated with the severity of GVHD but positively correlated with recent thymic emigrants. The results suggest that defective thymic function contributes to the impaired reconstitution of immune regulatory mechanisms following transplantation. The decrease in regulatory mechanisms post-transplant appears to provide an environment permissive to the development of GVHD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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