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This Article Full Text Full Text (PDF) 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 de Andrés, B. Articles by Lynch, R. G. Search for Related Content PubMed PubMed Citation Articles by de Andrés, B. Articles by Lynch, R. G. Related Collections Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  FcRII (CD32) Is Linked to Apoptotic Pathways in Murine Granulocyte Precursors and Mature Eosinophils Belen de Andrés, Allen L. Mueller, Arthur Blum, Joel Weinstock, Sjef Verbeek, Matyas Sandor, and Richard G. Lynch From the Department of Pathology and Department of Internal Medicine, University of Iowa, Iowa City, IA; Department of Immunology, University Hospital Utrecht, Utrecht, The Netherlands; and Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, WI. Murine granulocytes and precursors express low-affinity IgG Fc receptors (FcR). We investigated the effects of FcR ligation on the development of eosinophils in cultures of normal murine bone marrow. Eosinophilopoiesis was induced by culture of bone marrow cells in the presence of cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin-3 [IL-3], and IL-5). Addition to the cultures of 2.4G2, a rat monoclonal antibody (mAb) that reacts with FcRII (CD32) and FcRIII (CD16), induced granulocyte apoptosis within 24 hours. Granulocytes in cultures that contained 2.4G2 showed chromatin condensation, binding of Annexin-V, and fas induction, and by electron microscopy, apoptosis was most commonly observed in cells of the eosinophil lineage. Since murine granulocytes can express both FcRII (CD32) and FcRIII (CD16), we investigated the effect of 2.4G2 on cultures of bone marrow obtained from FcRIII (CD16) gene-disrupted mice and found that the apoptosis induced with 2.4G2 was CD16-independent. Studies with bone marrow cultures from B6MLR-lpr/lpr and C3H/HEJ-gld/gld mice established that the FcRII (CD32)-triggered apoptosis was fas-fasL-dependent. When mature eosinophils isolated from hepatic granulomas of Schistosoma mansoni-infected mice were cultured in cytokines in the presence of 2.4G2, the eosinophils underwent apoptosis within 24 hours. These findings identify a previously unknown linkage between FcR on eosinophils and fas-mediated apoptosis, a connection that could be relevant to mechanisms by which eosinophils mediate tissue injury and antibody-dependent cellular cytotoxicity reactions. Blood, Vol. 90 No. 3 (August 1), 1997: pp. 1267-1274 © 1997 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: K. Machida, H. Inoue, K. Matsumoto, M. Tsuda, S. Fukuyama, H. Koto, H. Aizawa, Y. Kureishi, N. Hara, and Y. Nakanishi Activation of PI3K-Akt pathway mediates antiapoptotic effects of {beta}-adrenergic agonist in airway eosinophils Am J Physiol Lung Cell Mol Physiol, May 1, 2005; 288(5): L860 - L867. [Abstract] [Full Text] [PDF] T. Watanabe, M. Okano, H. Hattori, T. Yoshino, N. Ohno, N. Ohta, Y. Sugata, Y. Orita, T. Takai, and K. Nishizaki Roles of Fc{gamma}RIIB in Nasal Eosinophilia and IgE Production in Murine Allergic Rhinitis Am. J. Respir. Crit. Care Med., January 1, 2004; 169(1): 105 - 112. [Abstract] [Full Text] [PDF] J. Schettini, G. Salamone, A. Trevani, S. Raiden, R. Gamberale, M. Vermeulen, M. Giordano, and J. R. Geffner Stimulation of neutrophil apoptosis by immobilized IgA J. Leukoc. Biol., October 1, 2002; 72(4): 685 - 691. [Abstract] [Full Text] [PDF] L. Chen, K. V. N. Rao, Y.-X. He, and K. Ramaswamy Skin-stage Schistosomula of Schistosoma mansoni Produce an Apoptosis-inducing Factor That Can Cause Apoptosis of T Cells J. Biol. Chem., September 6, 2002; 277(37): 34329 - 34335. [Abstract] [Full Text] [PDF] M. A. Giembycz and M. A. Lindsay Pharmacology of the Eosinophil Pharmacol. Rev., June 1, 1999; 51(2): 213 - 340. [Abstract] [Full Text] [PDF] J.-T. Kim, A. W. Schimming, and H. Kita Ligation of Fc{gamma}RII (CD32) Pivotally Regulates Survival of Human Eosinophils J. Immunol., April 1, 1999; 162(7): 4253 - 4259. [Abstract] [Full Text] [PDF] C. A. Rumbley, H. Sugaya, S. A. Zekavat, M. El Refaei, P. J. Perrin, and S. M. Phillips Activated Eosinophils Are the Major Source of Th2-Associated Cytokines in the Schistosome Granuloma J. Immunol., January 15, 1999; 162(2): 1003 - 1009. [Abstract] [Full Text] [PDF] B. de Andres, A. L. Mueller, S. Verbeek, M. Sandor, and R. G. Lynch A Regulatory Role for Fcgamma Receptors CD16 and CD32 in the Development of Murine B Cells Blood, October 15, 1998; 92(8): 2823 - 2829. [Abstract] [Full Text] [PDF] R. Gamberale, M. Giordano, A. S. Trevani, G. Andonegui, and J. R. Geffner Modulation of Human Neutrophil Apoptosis by Immune Complexes J. Immunol., October 1, 1998; 161(7): 3666 - 3674. [Abstract] [Full Text] [PDF]

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