SEARCH:   Advanced

Blood, 1 December 2005, Vol. 106, No. 12, pp. 3955-3957. Prepublished online as a Blood First Edition Paper on August 11, 2005; DOI 10.1182/blood-2004-09-3749. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-09-3749v1 106/12/3955    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 Kloosterboer, F. M. Articles by Falkenburg, J. H. F. Search for Related Content PubMed PubMed Citation Articles by Kloosterboer, F. M. Articles by Falkenburg, J. H. F. Related Collections Immunobiology Neoplasia Transfusion Medicine Immunotherapy Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief report Up-regulated expression in nonhematopoietic tissues of the BCL2A1-derived minor histocompatibility antigens in response to inflammatory cytokines: relevance for allogeneic immunotherapy of leukemia Freke M. Kloosterboer, Simone A. P. van Luxemburg-Heijs, Ronald A. van Soest, H. M. Esther van Egmond, Roel Willemze, and J. H. Frederik Falkenburg From the Department of Hematology, Leiden University Medical Center, Leiden, The Netherlands. T cells directed against hematopoietic-restricted minor histocompatibility antigens (mHags) may mediate graft-versus-leukemia (GVL) reactivity without graft-versus-host disease (GVHD). Recently, the HLA-A24–restricted mHag ACC-1 and the HLA-B44–restricted mHag ACC-2 encoded by separate polymorphisms within the BCL2A1 gene were characterized. Hematopoietic-restricted expression was suggested for these mHags. We demonstrate BCL2-related protein A1 (BCL2A1) mRNA expression in mesenchymal stromal cells (MSCs) that was up-regulated by the inflammatory cytokines tumor necrosis factor (TNF-) and/or interferon (IFN-). Analysis of cytotoxicity and IFN- production illustrated that ACC-2–specific T cells did not recognize untreated MSCs or IFN-–treated MSCs but showed specific recognition and killing of MSCs treated with TNF- plus IFN-. We hypothesize that under steady-state circumstances BCL2A1-specific T cells may exhibit relative specificity for hematopoietic tissue, but reactivity against nonhematopoietic cells may occur when inflammatory infiltrates are present. Thus, the role of BCL2A1-specific T cells in differential induction of GVL reactivity and GVHD may depend on the presence of inflammatory responses that may occur during GVHD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. M. van Bergen, M. G. D. Kester, I. Jedema, M. H. M. Heemskerk, S. A. P. van Luxemburg-Heijs, F. M. Kloosterboer, W. A. E. Marijt, A. H. de Ru, M. R. Schaafsma, R. Willemze, et al. Multiple myeloma-reactive T cells recognize an activation-induced minor histocompatibility antigen encoded by the ATP-dependent interferon-responsive (ADIR) gene Blood, May 1, 2007; 109(9): 4089 - 4096. [Abstract] [Full Text] [PDF] D. Blaise, N. Vey, C. Faucher, and M. Mohty Current status of reduced intensity conditioning allogeneic stem cell transplantation for acute myeloid leukemia Haematologica, April 1, 2007; 92(4): 533 - 541. [Abstract] [Full Text] [PDF]

	Copyright © 2005 by American Society of Hematology         Online ISSN: 1528-0020