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Blood, 15 February 2004, Vol. 103, No. 4, pp. 1542-1547. Prepublished online as a Blood First Edition Paper on October 16, 2003; DOI 10.1182/blood-2003-03-0957. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-03-0957v1 103/4/1542    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Petrovic, A. Articles by van den Brink, M. R. M. Search for Related Content PubMed PubMed Citation Articles by Petrovic, A. Articles by van den Brink, M. R. M. Related Collections Immunobiology Transplantation Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSPLANTATION LPAM (47 integrin) is an important homing integrin on alloreactive T cells in the development of intestinal graft-versus-host disease Aleksandra Petrovic, Onder Alpdogan, Lucy M. Willis, Jeffrey M. Eng, Andrew S. Greenberg, Barry J. Kappel, Chen Liu, George J. Murphy, Glenn Heller, and Marcel R. M. van den Brink From the Department of Pediatrics and Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY; Department of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville; Department of Pathology, Thomas Jefferson Medical Center, Philadelphia, PA; and Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY. Lymphocyte Peyer patch adhesion molecule (LPAM) or 47 integrin is expressed on lymphocytes and is responsible for T-cell homing into gut-associated lymphoid tissues through its binding to mucosal addressin cell adhesion molecule (MAdCAM), which is present on high endothelial venules of mucosal lymphoid organs. We found in murine allogeneic bone marrow transplantation (BMT) models that recipients of 47– donor T cells had significantly less graft-versus-host disease (GVHD) morbidity and mortality compared with recipients of 47+ donor T cells. A kinetic posttransplantation analysis of lymphocytes in the intestines and mesenteric lymph nodes demonstrated a delayed invasion of lower numbers of 47+ T cells in recipients of 47– T cells compared with recipients of 47+ T cells. Histopathologic analysis of GVHD target organs revealed that recipients of 47– T cells developed less GVHD of the intestines and liver, whereas there was no difference in cutaneous and thymic GVHD between recipients of 47– or 47+ T cells. Finally, we found that in vivo GVT activity of 47– donor T cells was preserved. We conclude that the 47 integrin is important for the invasion of alloreactive donor T cells into the gut and the subsequent development of intestinal GVHD and overall GVHD morbidity and mortality. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. W. Kappel, G. L. Goldberg, C. G. King, D. Y. Suh, O. M. Smith, C. Ligh, A. M. Holland, J. Grubin, N. M. Mark, C. Liu, et al. IL-17 contributes to CD4-mediated graft-versus-host disease Blood, January 22, 2009; 113(4): 945 - 952. 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