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Blood, 29 October 2009, Vol. 114, No. 18, pp. 3909-3916. Prepublished online as a Blood First Edition Paper on August 26, 2009; DOI 10.1182/blood-2009-02-206946. This Article Full Text Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2009-02-206946v1 114/18/3909    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 CrossRef Google Scholar Articles by Le Dieu, R. Articles by Gribben, J. G. PubMed PubMed Citation Articles by Le Dieu, R. Articles by Gribben, J. G. Related Collections Immunobiology Myeloid Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  MYELOID NEOPLASIA Peripheral blood T cells in acute myeloid leukemia (AML) patients at diagnosis have abnormal phenotype and genotype and form defective immune synapses with AML blasts Rifca Le Dieu1,*, David C. Taussig1,*, Alan G. Ramsay1,*, Richard Mitter2, Faridah Miraki-Moud1, Rewas Fatah1, Abigail M. Lee1, T. Andrew Lister1, and John G. Gribben1 1 Institute of Cancer, Centre for Medical Oncology, Barts and The London School of Medicine, Queen Mary University of London, London; and 2 Bioinformatics and Biostatistics Service, Cancer Research UK, London, United Kingdom Understanding how the immune system in patients with cancer interacts with malignant cells is critical for the development of successful immunotherapeutic strategies. We studied peripheral blood from newly diagnosed patients with acute myeloid leukemia (AML) to assess the impact of this disease on the patients' T cells. The absolute number of peripheral blood T cells is increased in AML compared with healthy controls. An increase in the absolute number of CD3+56+ cells was also noted. Gene expression profiling on T cells from AML patients compared with healthy donors demonstrated global differences in transcription suggesting aberrant T-cell activation patterns. These gene expression changes differ from those observed in chronic lymphocytic leukemia (CLL), indicating the heterogeneous means by which different tumors evade the host immune response. However, in common with CLL, differentially regulated genes involved in actin cytoskeletal formation were identified, and therefore the ability of T cells from AML patients to form immunologic synapses was assessed. Although AML T cells could form conjugates with autologous blasts, their ability to form immune synapses and recruit phosphotyrosine signaling molecules to the synapse was significantly impaired. These findings identify T-cell dysfunction in AML that may contribute to the failure of a host immune response against leukemic blasts. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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