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Blood, 15 December 2004, Vol. 104, No. 13, pp. 4236-4244. Prepublished online as a Blood First Edition Paper on August 24, 2004; DOI 10.1182/blood-2004-06-2229. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-06-2229v1 2004-06-2229v2 104/13/4236    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 Krause, D. S. Articles by Van Etten, R. A. Search for Related Content PubMed PubMed Citation Articles by Krause, D. S. Articles by Van Etten, R. A. Related Collections Neoplasia Oncogenes and Tumor Suppressors Immunotherapy Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Adoptive immunotherapy of BCR-ABL–induced chronic myeloid leukemia–like myeloproliferative disease in a murine model Daniela S. Krause, and Richard A. Van Etten From the CBR (Center for Blood Research) Institute for Biomedical Research, Harvard Medical School, Boston, MA; and the Molecular Oncology Research Institute, Tufts–New England Medical Center, Boston, MA. Donor leukocyte infusion (DLI) can induce graft-versus-leukemia (GvL) reactions in patients with chronic myeloid leukemia (CML) relapsing after allogeneic bone marrow transplantation (BMT), but the mechanisms of the antileukemic effect of DLI are unknown, and the procedure is complicated by graft-versus-host disease (GvHD) and graft failure. Here, we adapted a murine retroviral BMT model of Philadelphia+ leukemia by combining allogeneic bone marrow (BM) from C57Bl/6 (H-2b) mice with BCR-ABL–transduced Balb/c (H-2d) BM, inducing mixed chimerism and myeloproliferative disease in recipients resembling relapse of CML following allogeneic BMT. Infusions of allogeneic splenocytes eliminated BCR-ABL–induced CML-like disease in the majority of mixed chimeras, with significant GvL effects mediated by both CD4+ and CD4- cells. BCR-ABL–induced acute B-lymphoblastic leukemia was also eradicated by DLI in major histocompatibility complex (MHC)–mismatched chimeras. Most DLI-treated mice converted to full allogeneic chimerism but succumbed frequently to GvHD or graft failure. When MHC-matched B10.D2 (H-2d) mice were the allogeneic donors, CML-like disease was more resistant to DLI. These results suggest that depletion of CD8+ cells from DLI could impair GvL against CML, while increased MHC disparity between donor and recipient may improve the responsiveness of Philadelphia+ B-lymphoblastic leukemia to DLI. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Adoptive immunotherapy of murine CML: navigating between Scylla and Charybdis Michael W. N. Deininger Blood 2004 104: 3843. [Full Text] [PDF] This article has been cited by other articles: V. Nardi, O. Naveiras, M. Azam, and G. Q. Daley ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines Blood, April 16, 2009; 113(16): 3813 - 3820. [Abstract] [Full Text] [PDF]

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