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Blood, 15 December 2006, Vol. 108, No. 13, pp. 3967-3975. Prepublished online as a Blood First Edition Paper on August 22, 2006; DOI 10.1182/blood-2006-04-020610. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-04-020610v1 108/13/3967    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 Bobé, P. Articles by Chelbi-Alix, M. K. Search for Related Content PubMed PubMed Citation Articles by Bobé, P. Articles by Chelbi-Alix, M. K. Related Collections Immunobiology Plenary Papers Signal Transduction Immunotherapy Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLENARY PAPERS Arsenic trioxide: a promising novel therapeutic agent for lymphoproliferative and autoimmune syndromes in MRL/lpr mice Pierre Bobé, Danielle Bonardelle, Karim Benihoud, Paule Opolon, and Mounira K. Chelbi-Alix From the Centre National de la Recherche Scientifique (CNRS) Unite Propre de Recherche (UPR) 9045, Villejuif, France; Université Paris-Sud XI, Orsay, France; and CNRS/Institut Gustave-Roussy, Unité Mixte de Recherche (UMR) 8121, Villejuif, France. MRL/lpr mice develop a human lupuslike syndrome and, as in autoimmune lymphoproliferative syndrome (ALPS), massive lymphoproliferation due to inactivation of Fas-mediated apoptosis. Presently, no effective therapy exists for ALPS, and long term, therapies for lupus are hazardous. We show herein that arsenic trioxide (As2O3) is able to achieve quasi-total regression of antibody- and cell-mediated manifestations in MRL/lpr mice. As2O3 activated caspases and eliminated the activated T lymphocytes responsible for lymphoproliferation and skin, lung, and kidney lesions, leading to significantly prolonged survival rates. This treatment also markedly reduced anti-DNA autoantibody, rheumatoid factor, IL-18, IFN-, nitric oxide metabolite, TNF-, Fas ligand, and IL-10 levels and immune-complex deposits in glomeruli. As2O3 restored cellular reduced glutathione levels, thereby limiting the toxic effect of nitric oxide, which is overproduced in MRL/lpr mice. Furthermore, As2O3 protected young animals against developing the syndrome and induced almost total disease disappearance in older affected mice, thereby demonstrating that it is a novel promising therapeutic agent for autoimmune diseases. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Poisoning autoimmunity Vito Pistoia Blood 2006 108: 3964-3965. [Full Text] [PDF] This article has been cited by other articles: T. B. Sundberg, L. Swenson, D. R. Wahl, A. W. Opipari Jr., and G. D. Glick Apoptotic Signaling Activated by Modulation of the F0F1-ATPase: Implications for Selective Killing of Autoimmune Lymphocytes J. Pharmacol. Exp. Ther., November 1, 2009; 331(2): 437 - 444. [Abstract] [Full Text] [PDF] D. T. Teachey, A. E. Seif, V. I. Brown, M. Bruno, R. M. Bunte, Y. J. Chang, J. K. Choi, J. D. Fish, J. Hall, G. S. Reid, et al. Targeting Notch signaling in autoimmune and lymphoproliferative disease Blood, January 15, 2008; 111(2): 705 - 714. [Abstract] [Full Text] [PDF] Arsenic Trioxide for Autoimmune Diseases? Journal Watch Oncology and Hematology, January 12, 2007; 2007(112): 5 - 5. [Full Text]

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