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Blood, 15 April 2007, Vol. 109, No. 8, pp. 3325-3332. Prepublished online as a Blood First Edition Paper on December 19, 2006; DOI 10.1182/blood-2006-04-017863. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-04-017863v1 109/8/3325    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 Woetmann, A. Articles by Ødum, N. Search for Related Content PubMed PubMed Citation Articles by Woetmann, A. Articles by Ødum, N. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Nonmalignant T cells stimulate growth of T-cell lymphoma cells in the presence of bacterial toxins Anders Woetmann1,2, Paola Lovato1,2, Karsten W. Eriksen1,2, Thorbjørn Krejsgaard1,2, Tord Labuda1,2, Qian Zhang3, Anne-Merethe Mathiesen1,2, Carsten Geisler2, Arne Svejgaard4, Mariusz A. Wasik3, and Niels Ødum1,2 1 Institute of Molecular Biology and 2 Institute of Medical Microbiology and Immunology, University of Copenhagen, Denmark; 3 Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia; 4 Department of Clinical Immunology, University Hospital of Copenhagen (Rigshospitalet), Denmark Bacterial toxins including staphylococcal enterotoxins (SEs) have been implicated in the pathogenesis of cutaneous T-cell lymphomas (CTCLs). Here, we investigate SE-mediated interactions between nonmalignant T cells and malignant T-cell lines established from skin and blood of CTCL patients. The malignant CTCL cells express MHC class II molecules that are high-affinity receptors for SE. Although treatment with SE has no direct effect on the growth of the malignant CTCL cells, the SE-treated CTCL cells induce vigorous proliferation of the SE-responsive nonmalignant T cells. In turn, the nonmalignant T cells enhance proliferation of the malignant cells in an SE- and MHC class II–dependent manner. Furthermore, SE and, in addition, alloantigen presentation by malignant CTCL cells to irradiated nonmalignant CD4+ T-cell lines also enhance proliferation of the malignant cells. The growth-promoting effect depends on direct cell-cell contact and soluble factors such as interleukin-2. In conclusion, we demonstrate that SE triggers a bidirectional cross talk between nonmalignant T cells and malignant CTCL cells that promotes growth of the malignant cells. This represents a novel mechanism by which infections with SE-producing bacteria may contribute to pathogenesis of CTCL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Krejsgaard, C. S. Vetter-Kauczok, A. Woetmann, H. Kneitz, K. W. Eriksen, P. Lovato, Q. Zhang, M. A. Wasik, C. Geisler, E. Ralfkiaer, et al. Ectopic expression of B-lymphoid kinase in cutaneous T-cell lymphoma Blood, June 4, 2009; 113(23): 5896 - 5904. [Abstract] [Full Text] [PDF]

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