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Blood, 15 May 2004, Vol. 103, No. 10, pp. 3982-3985. Prepublished online as a Blood First Edition Paper on February 5, 2004; DOI 10.1182/blood-2003-05-1735. This Article Full Text (PDF) All Versions of this Article: 2003-05-1735v1 103/10/3982    most recent Alert me when this article is cited Alert me if a correction is posted 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 Lang, P. Articles by Fey, G. H Search for Related Content PubMed PubMed Citation Articles by Lang, P. Articles by Fey, G. H Social Bookmarking                   What's this? Submitted May 30, 2003 Accepted January 22, 2004 A chimeric CD19 antibody mediates cytotoxic activity against leukemic blasts with effectors from pediatric patients transplanted with T cell depleted allografts Peter Lang*, Karin Barbin, Tobias Feuchtinger, Johan Greil, Matthias Peipp, Susan J Zunino, Matthias Pfeiffer, Rupert Handgretinger, Dietrich Niethammer, and Georg H Fey Pediatric Oncology, University Children's Hospital, Tuebingen, Germany Chair of Genetics, University of Erlangen-Nuremberg, Erlangen, Germany Stem Cell Transplantation Unit, St Jude Children's Research Hospital, Memphis, TN, USA * Corresponding author; email: prlang{at}med.uni-tuebingen.de. Relapse is a major problem after transplantation in children with acute B-lineage leukemias, and new therapies are needed to increase graft versus leukemia effects (GvL) without inducing graft versus host disease (GvHD). Here we studied the ability of effector cells recovered from patients transplanted with positive selected stem cells from alternative donors to induce antibody dependent cellular cytotoxicity (ADCC). For this purpose, a chimeric CD19 antibody, CD19-4G7chim, was generated. This antibody efficiently mediated ADCC against primary ALL blasts using purified NK cells from healthy donors or mononuclear cells from transplanted patients as effector cells. Increased lysis was obtained after stimulation of effector cells with interleukin-2 (IL-2). ADCC was not prevented by inhibitory effects mediated by HLA class I. We propose that treatment with chimeric CD19 antibodies leading to ADCC by donor-derived NK cells may become a therapeutic option for the post-transplantation treatment of minimal residual B-lineage ALLs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Kugler, C. Stein, M. Schwenkert, D. Saul, L. Vockentanz, T. Huber, S. K. Wetzel, O. Scholz, A. Pluckthun, A. Honegger, et al. Stabilization and humanization of a single-chain Fv antibody fragment specific for human lymphocyte antigen CD19 by designed point mutations and CDR-grafting onto a human framework Protein Eng. Des. Sel., March 1, 2009; 22(3): 135 - 147. [Abstract] [Full Text] [PDF] P. Bader, H. Kreyenberg, G. H.R. Henze, C. Eckert, M. Reising, A. Willasch, A. Barth, A. Borkhardt, C. Peters, R. Handgretinger, et al. Prognostic Value of Minimal Residual Disease Quantification Before Allogeneic Stem-Cell Transplantation in Relapsed Childhood Acute Lymphoblastic Leukemia: The ALL-REZ BFM Study Group J. Clin. Oncol., January 20, 2009; 27(3): 377 - 384. [Abstract] [Full Text] [PDF] C. T. Rankin, M.-C. Veri, S. Gorlatov, N. Tuaillon, S. Burke, L. Huang, H. D. Inzunza, H. Li, S. Thomas, S. Johnson, et al. CD32B, the human inhibitory Fc-{gamma} receptor IIB, as a target for monoclonal antibody therapy of B-cell lymphoma Blood, October 1, 2006; 108(7): 2384 - 2391. [Abstract] [Full Text] [PDF]

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