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Blood, 1 January 2005, Vol. 105, No. 1, pp. 428-431. Prepublished online as a Blood First Edition Paper on August 26, 2004; DOI 10.1182/blood-2004-01-0371. This Article Full Text (PDF) All Versions of this Article: 2004-01-0371v1 105/1/428    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 Gendelman, M. Articles by Drobyski, W. R Search for Related Content PubMed PubMed Citation Articles by Gendelman, M. Articles by Drobyski, W. R Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 29, 2004 Accepted August 11, 2004 Phenyl-N-TERT-Butylnitrone (PBN) protects syngeneic marrow transplant recipients from the lethal cytokine syndrome occurring after agonistic CD40 antibody administration Maria Gendelman, Nadine Halligan, Richard Komorowski, Brent Logan, William J Murphy, Bruce R Blazar, Kirkwood A Pritchard Jr., and William R Drobyski* Departments of Medicine, Bone Marrow Transplant Program, Medical College of Wisconsin, Milwaukee, WI, USA Department of Pathology, Bone Marrow Transplant Program, Medical College of Wisconsin, Milwaukee, WI, USA Department of Biostatistics, Bone Marrow Transplant Program, Medical College of Wisconsin, Milwaukee, WI, USA Department of Microbiology and Immunology, University of Nevada-Reno, Reno, NV, USA Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA Department of Pediatric Surgery, Bone Marrow Transplant Program, Medical College of Wisconsin, Milwaukee, WI, USA * Corresponding author; email: bill{at}bmt.mcw.edu. Administration of agonistic monoclonal antibodies or recombinant cytokines is a potential approach to enhance antitumor immunity in bone marrow transplant (BMT) recipients, but is complicated by toxicity due to proinflammatory cytokine-mediated vital organ damage. We employed a murine syngeneic BMT model in which administration of anti-CD40 antibody early post-BMT results in overproduction of IL-12 and IFN- and lethal gut toxicity to examine the protective effect of the spin trap inhibitor, alpha phenyl-tert-butylnitrone (PBN). Administration of PBN protected transplant recipients from mortality by significantly attenuating gut toxicity, but did not effect a reduction in the levels of proinflammatory cytokines (IL-12, IFN-, TNF-, or nitrate/nitrite). Moreover, PBN did not compromise anti-CD40 antibody-mediated antitumor effects in a nontransplant lymphoma model. Collectively, these data suggest that PBN administration may represent a novel approach for reduction of toxicity without compromise of antitumor effects resulting from administration of therapeutic antibodies in both transplant and nontransplant settings. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. R. French, V. Y. Taraban, G. R. Crowther, T. F. Rowley, J. C. Gray, P. W. Johnson, A. L. Tutt, A. Al-Shamkhani, and M. J. Glennie Eradication of lymphoma by CD8 T cells following anti-CD40 monoclonal antibody therapy is critically dependent on CD27 costimulation Blood, June 1, 2007; 109(11): 4810 - 4815. [Abstract] [Full Text] [PDF]

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