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Prepublished online as a Blood First Edition Paper on July 5, 2002; DOI 10.1182/blood-2002-01-0174. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-01-0174v1 100/4/1373    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 Chen, Y. Articles by Jadus, M. R. Search for Related Content PubMed PubMed Citation Articles by Chen, Y. Articles by Jadus, M. R. Related Collections Immunobiology Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 August 2002, Vol. 100, No. 4, pp. 1373-1380 IMMUNOBIOLOGY Living T9 glioma cells expressing membrane macrophage colony-stimulating factor produce immediate tumor destruction by polymorphonuclear leukocytes and macrophages via a "paraptosis"-induced pathway that promotes systemic immunity against intracranial T9 gliomas Yijun Chen, Thomas Douglass, Edward W. B. Jeffes, Qingcheng Xu, Christopher C. Williams, Neary Arpajirakul, Christina Delgado, Michael Kleinman, Ramon Sanchez, Qinghong Dan, Ronald C. Kim, H. Terry Wepsic, and Martin R. Jadus From the Diagnostic and Molecular Health Care Group and the Dermatology Service, Veterans Affairs Medical Center, Long Beach, CA; the Pathology Department, the Department of Community and Environmental Medicine, and the Department of Dermatology, University of California, Irvine; and the Biological Sciences Department, California State University, Long Beach. Cloned T9-C2 glioma cells transfected with membrane macrophage colony-stimulating factor (mM-CSF) never formed subcutaneous tumors when implanted into Fischer rats, whereas control T9 cells did. The T9-C2 cells were completely killed within 1 day through a mechanism that resembled paraptosis. Vacuolization of the T9-C2 cell's mitochondria and endoplasmic reticulum started within 4 hours after implantation. By 24 hours, the dead tumor cells were swollen and terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL)-positive. Bcl2-transduced T9-C2 cells failed to form tumors in rats. Both T9 and T9-C2 cells produced cytokine-induced neutrophil chemoattractant that recruited the granulocytes into the tumor injection sites, where they interacted with the tumor cells. Freshly isolated macrophages killed the T9-C2 cells in vitro by a mechanism independent of phagocytosis. Nude athymic rats treated with antiasialo GM1 antibody formed T9-C2 tumors, whereas rats treated with a natural killer cell (NK)-specific antibody failed to form tumors. When treated with antipolymorphonuclear leukocyte (anti-PMN) and antimacrophage antibodies, 80% of nude rats formed tumors, whereas only 40% of the rats developed a tumor when a single antibody was used. This suggests that both PMNs and macrophages are involved in the killing of T9-C2 tumor cells. Immunocompetent rats that rejected the living T9-C2 cells were immune to the intracranial rechallenge with T9 cells. No vaccinating effect occurred if the T9-C2 cells were freeze-thawed, x-irradiated, or treated with mitomycin-C prior to injection. Optimal tumor immunization using mM-CSF-transduced T9 cells requires viable tumor cells. In this study optimal tumor immunization occurred when a strong inflammatory response at the injection of the tumor cells was induced. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Tardito, C. Isella, E. Medico, L. Marchio, E. Bevilacqua, M. Hatzoglou, O. Bussolati, and R. Franchi-Gazzola The Thioxotriazole Copper(II) Complex A0 Induces Endoplasmic Reticulum Stress and Paraptotic Death in Human Cancer Cells J. Biol. Chem., September 4, 2009; 284(36): 24306 - 24319. [Abstract] [Full Text] [PDF] T. Dvorkin, X. Song, S. Argov, R. M. White, M. Zoller, S. Segal, C. A. Dinarello, E. Voronov, and R. N. 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