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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 (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 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 Related Article in Blood Online Social Bookmarking                   What's this? Submitted August 27, 2003 Accepted December 3, 2003 The quantity and duration of FcR signals determines mast cell degranulation and survival Sho Yamasaki, Eri Ishikawa, Masayuki Kohno, and Takashi Saito* Department of Molecular Genetics, Graduate School of Medicine, Chiba University, Chiba, Japan Laboratory of Cell Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan * Corresponding author; email: saito{at}med.m.chiba-u.ac.jp. 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 in bone marrow-derived mast cells (BMMCs) from FcR-/- mice to manipulate the strength of FcR signals by anti-CD8 crosslinking. Crosslinking of CD8/ induced mast cell survival and degranulation. Survival was induced by weaker stimulation than needed for degranulation, from the analysis by varying anti-CD8 concentrations or using monomeric CD8/ mutants. However, sustained Erk activation seems to regulate survival even when the activation signal was strong enough to elicit degranulation. Generation of sustained Erk activation by active MEK induced BMMC survival. These results suggest that the duration and the magnitude of FcR signals may determine mast cell survival and degranulation, respectively. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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