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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4669-4677. Prepublished online as a Blood First Edition Paper on March 2, 2006; DOI 10.1182/blood-2005-09-3775. This Article Full Text (PDF) All Versions of this Article: 2005-09-3775v1 107/12/4669    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 Clemenceau, B. Articles by Vie, H. Search for Related Content PubMed PubMed Citation Articles by Clemenceau, B. Articles by Vie, H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 21, 2005 Accepted February 15, 2006 Antibody-Dependent Cellular Cytotoxicity (ADCC) mediated by genetically modified antigen-specific human T lymphocytes Beatrice Clemenceau, Nicolas Conjy-Jolivet, Geraldine Gallot, Regine Vivien, Joelle Gaschet, Gilles Thibault, and Henri Vie* INSERM U601, Centre Hospitalier Universitaire de Nantes, Nantes, France Laboratoire d'Immunologie, Faculte de Medecine, Universite Francois Rabelais, Tours, France * Corresponding author; email: hvie{at}nantes.inserm.fr. In the context of transplantation, donor and virus-specific T-lymphocytes infusions have demonstrated the dramatic potential of T cells as immune effectors. Unfortunately, most attempts to exploit the T cell immune system against non-viral malignancies in the syngeneic setting have been disappointing. In contrast treatments based on monoclonal antibodies (Abs) have been clinically successful and have demonstrated the clinical relevance of several antigens as therapeutic targets and the importance of the antibody dependant cellular cytotoxicity (ADCC) pathway. In the present study we considered the possibility of arming specific T cells with a receptor that would enable them to mediate ADCC. After transduction with a CD16/ receptor gene, CD4+ and CD8+ cytotoxic T lymphocytes displayed stable expression of the CD16 receptor at their surface. In the absence of Ab, CD16/ expression did not affect the capacity of specific T-lymphocytes to kill their target following "natural" T cell receptor recognition. When tested against the autologous B lymphoblastoid cell line (BLCL) coated with anti-CD20 mAb, the newly expressed Fc receptor enabled the T cells to kill the BLCL through ADCC. Adoptive transfer of such newly designed immune effector may be considered to increase antibody efficiency by harnessing the immune potential of T cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Hudrisier, B. Clemenceau, S. Balor, S. Daubeuf, E. Magdeleine, M. Daeron, P. Bruhns, and H. Vie Ligand Binding but Undetected Functional Response of FcR after Their Capture by T Cells via Trogocytosis J. Immunol., November 15, 2009; 183(10): 6102 - 6113. [Abstract] [Full Text] [PDF] N. K. Bjorkstrom, V. D. Gonzalez, K.-J. Malmberg, K. Falconer, A. Alaeus, G. Nowak, C. Jorns, B.-G. Ericzon, O. Weiland, J. K. Sandberg, et al. Elevated Numbers of Fc{gamma}RIIIA+ (CD16+) Effector CD8 T Cells with NK Cell-Like Function in Chronic Hepatitis C Virus Infection J. Immunol., September 15, 2008; 181(6): 4219 - 4228. [Abstract] [Full Text] [PDF]

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