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Blood, 1 July 2007, Vol. 110, No. 1, pp. 9-17. Prepublished online as a Blood First Edition Paper on February 27, 2007; DOI 10.1182/blood-2006-12-022038. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-12-022038v1 110/1/9    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 Chakraverty, R. Articles by Sykes, M. Search for Related Content PubMed PubMed Citation Articles by Chakraverty, R. Articles by Sykes, M. Related Collections Immunobiology Transplantation Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW ARTICLE The role of antigen-presenting cells in triggering graft-versus-host disease and graft-versus-leukemia Ronjon Chakraverty1, and Megan Sykes2 1 Department of Hematology, University College London, London, United Kingdom; 2 Transplantation Biology Research Center, Bone Marrow Transplantation Section, Massachusetts General Hospital, Harvard Medical School, Boston, MA After allogeneic blood or bone marrow transplantation, donor T cells interact with a distorted antigen-presenting cell (APC) environment in which some, but not all, host APCs are replaced by APCs from the donor. Significantly, host APCs are required for the priming of acute graft-versus-host disease (GVHD). Donor APCs play a lesser role in the induction of acute GVHD despite their predicted capacity to cross-present host antigens. In contrast, donor APCs may play a role in perpetuating the tissue injury observed in chronic GVHD. Host APCs are also required for maximal graft-versus-leukemia responses. Recent studies have suggested potential strategies by which the continued presence of host APCs can be exploited to prime strong donor immunity to tumors without the induction of GVHD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Zhao, C. Zhang, T. Yi, C.-L. Lin, I. Todorov, F. Kandeel, S. Forman, and D. Zeng In vivo-activated CD103+CD4+ regulatory T cells ameliorate ongoing chronic graft-versus-host disease Blood, September 1, 2008; 112(5): 2129 - 2138. [Abstract] [Full Text] [PDF] T. Yi, D. Zhao, C.-L. Lin, C. Zhang, Y. Chen, I. Todorov, T. LeBon, F. Kandeel, S. Forman, and D. Zeng Absence of donor Th17 leads to augmented Th1 differentiation and exacerbated acute graft-versus-host disease Blood, September 1, 2008; 112(5): 2101 - 2110. [Abstract] [Full Text] [PDF] A. Shimabukuro-Vornhagen, T. Liebig, and M. von Bergwelt-Baildon Statins inhibit human APC function: implications for the treatment of GVHD Blood, August 15, 2008; 112(4): 1544 - 1545. [Full Text] [PDF] T. D. Kim, T. H. Terwey, J. L. Zakrzewski, D. Suh, A. A. Kochman, M. E. Chen, C. G. King, C. Borsotti, J. Grubin, O. M. Smith, et al. Organ-derived dendritic cells have differential effects on alloreactive T cells Blood, March 1, 2008; 111(5): 2929 - 2940. [Abstract] [Full Text] [PDF]

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