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Blood, 15 April 2004, Vol. 103, No. 8, pp. 3093-3101. Prepublished online as a Blood First Edition Paper on December 11, 2003; DOI 10.1182/blood-2003-08-2944. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2944v1 103/8/3093    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 Yamasaki, S. Articles by Saito, T. Search for Related Content PubMed PubMed Citation Articles by Yamasaki, S. Articles by Saito, T. Related Collections Immunobiology Apoptosis Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY The quantity and duration of FcR signals determine mast cell degranulation and survival Sho Yamasaki, Eri Ishikawa, Masayuki Kohno, and Takashi Saito From the Department of Molecular Genetics (H1), Graduate School of Medicine, Chiba University, Chiba, Japan; and Laboratory of Cell Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan. Immunoglobulin E (IgE) bound to multivalent antigen (Ag) elicits mast cell degranulation but not survival; on the contrary, IgE in the absence of Ag (IgE(-Ag)) induces survival only but not degranulation. Although these distinct responses are mediated through the same receptor, FcRI, the molecular mechanism generating the divergence is largely unknown. We recently showed that the signals through FcR chain are essential for IgE(-Ag)–induced mast cell survival as well as IgE(+Ag)–induced degranulation. To determine whether the cellular output is regulated by the quantity of FcR signal, we expressed CD8/FcR chimeras (CD8/) in bone marrow–derived mast cells (BMMCs) from FcR-/- mice to manipulate the strength of FcR signals by anti-CD8 cross-linking. Cross-linking of CD8/ induced mast cell survival and degranulation. Survival was induced by weaker stimulation than needed for degranulation in terms of anti-CD8 concentration and the valency of chimera. However, sustained extracellular signal-regulated kinase (Erk) activation seems to regulate survival even when the activation signal was strong enough to elicit degranulation. Generation of sustained Erk activation by active mitogen-activated protein kinase kinase (MEK) induced BMMC survival. These results suggest that the duration and the magnitude of FcR signals may determine mast cell survival and degranulation, respectively. (Blood. 2004;103:3093-3101) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: IgE-induced signaling: only the weak survive Gerald Krystal Blood 2004 103: 2868-2869. [Full Text] [PDF] This article has been cited by other articles: N. H. Fifadara, C. C. Aye, S. K. Raghuwanshi, R. M. Richardson, and S. J. Ono CCR1 expression and signal transduction by murine BMMC results in secretion of TNF-{alpha}, TGF{beta}-1 and IL-6 Int. Immunol., August 1, 2009; 21(8): 991 - 1001. [Abstract] [Full Text] [PDF] H. Oda, M. Fujimoto, M. S. Patrick, D. Chida, Y. Sato, Y. Azuma, H. Aoki, T. Abe, H. Suzuki, and M. Shirai RhoH Plays Critical Roles in Fc{epsilon}RI-Dependent Signal Transduction in Mast Cells J. Immunol., January 15, 2009; 182(2): 957 - 962. [Abstract] [Full Text] [PDF] E. J. Rios, A. M. 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[Abstract] [Full Text] [PDF] M. Kohno, S. Yamasaki, V. L. J. Tybulewicz, and T. Saito Rapid and large amount of autocrine IL-3 production is responsible for mast cell survival by IgE in the absence of antigen Blood, March 1, 2005; 105(5): 2059 - 2065. [Abstract] [Full Text] [PDF]

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