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Blood, 1 October 2006, Vol. 108, No. 7, pp. 2485-2492. Prepublished online as a Blood First Edition Paper on June 20, 2006; DOI 10.1182/blood-2006-04-016063. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-04-016063v1 108/7/2485    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 Rowe, V. Articles by Hill, G. R. Search for Related Content PubMed PubMed Citation Articles by Rowe, V. Articles by Hill, G. R. Related Collections Transplantation Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSPLANTATION Host B cells produce IL-10 following TBI and attenuate acute GVHD after allogeneic bone marrow transplantation Vanessa Rowe, Tatjana Banovic, Kelli P. MacDonald, Rachel Kuns, Alistair L. Don, Edward S. Morris, Angela C. Burman, Helen M. Bofinger, Andrew D. Clouston, and Geoffrey R. Hill From The Queensland Institute of Medical Research; the Department of Stem Cell Transplantation, Royal Brisbane Hospital; the Department of Pathology, University of Queensland, Brisbane, Australia. Host antigen-presenting cells (APCs) are known to be critical for the induction of graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation (BMT), but the relative contribution of specific APC subsets remains unclear. We have studied the role of host B cells in GVHD by using B-cell–deficient µMT mice as BMT recipients in a model of CD4-dependent GVHD to major histocompatibility complex antigens. We demonstrate that acute GVHD is initially augmented in µMT recipients relative to wild-type recipients (mortality: 85% vs 44%, P < .01), and this is the result of an increase in donor T-cell proliferation, expansion, and inflammatory cytokine production early after BMT. Recipient B cells were depleted 28-fold at the time of BMT by total body irradiation (TBI) administered 24 hours earlier, and we demonstrate that TBI rapidly induces sustained interleukin-10 (IL-10) generation from B cells but not dendritic cells (DCs) or other cellular populations within the spleen. Finally, recipient mice in which B cells are unable to produce IL-10 due to homologous gene deletion develop more severe acute GVHD than recipient mice in which B cells are wild type. Thus, the induction of IL-10 in host B cells during conditioning attenuates experimental acute GVHD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Fehr, F. Haspot, J. Mollov, M. Chittenden, T. Hogan, and M. Sykes Alloreactive CD8 T Cell Tolerance Requires Recipient B Cells, Dendritic Cells, and MHC Class II J. Immunol., July 1, 2008; 181(1): 165 - 173. [Abstract] [Full Text] [PDF] R. Chakraverty and M. Sykes The role of antigen-presenting cells in triggering graft-versus-host disease and graft-versus-leukemia Blood, July 1, 2007; 110(1): 9 - 17. [Abstract] [Full Text] [PDF] H. J. Deeg How I treat refractory acute GVHD Blood, May 15, 2007; 109(10): 4119 - 4126. [Abstract] [Full Text] [PDF]

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