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Blood, 1 March 2005, Vol. 105, No. 5, pp. 2059-2065. Prepublished online as a Blood First Edition Paper on November 12, 2004; DOI 10.1182/blood-2004-07-2639. This Article Full Text (PDF) All Versions of this Article: 2004-07-2639v1 105/5/2059    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 Kohno, M. Articles by Saito, T. Search for Related Content PubMed PubMed Citation Articles by Kohno, M. Articles by Saito, T. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 13, 2004 Accepted November 1, 2004 Rapid and large amount of autocrine IL-3 production is responsible for mast cell survival by IgE in the absence of antigen Masayuki Kohno, Sho Yamasaki*, Victor L Tybulewicz, and Takashi Saito Department of Molecular Genetics, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan Department of Molecular Genetics, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan; Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, Tsurumi-ku, Yokohama, Japan Division of Immune Cell Biology, National Institute for Medical Research, London, United Kingdom * Corresponding author; email: sho{at}rcai.riken.jp. Crosslinking FcRI on mast cells by IgE and antigen initiates cascades leading to anti-parasitic or allergic responses. It was recently reported that IgE without antigen (IgE(-Ag)) actively promotes mast cell survival. Although we have demonstrated that the ITAM within FcR is essential for IgE(-Ag)-induced mast cell survival, the underlying mechanism remains still unclear. Here, we investigated the mechanism of IgE(-Ag)-induced survival using mast cells lacking several downstream molecules. Lyn and Syk were essential, whereas Fyn, Gab2 and the PI3K-Akt pathway were not critical for survival. Failure of survival in FcR-/- BMMCs was rescued by co-culture with IgE-treated WT BMMCs, suggesting that survival is induced not directly through FcRI signals. We found that the survival is predominantly mediated by high production of IL-3, evidenced by severe impairment of survival by anti-IL-3 and in IL-3-/- BMMCs. The upregulation of Bcl-xL/Bcl-2 by IgE was abrogated in IL-3-/- BMMCs, whreas the expression of histidine decarboxylase (HDC) was normally induced. These results indicate that IL-3 plays a crucial role for IgE(-Ag)-induced mast cell survival, functioning in an autocrine manner by inducing the Bcl-xL/Bcl-2 via STAT5. We further suggest that IgE(-Ag)-mediated gene expression in mast cells is regulated at least two mechanisms: autocrine IL-3-dependent and -independent. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Kambayashi, E. J. Allenspach, J. T. Chang, T. Zou, J. E. Shoag, S. L. Reiner, A. J. Caton, and G. A. Koretzky Inducible MHC Class II Expression by Mast Cells Supports Effector and Regulatory T Cell Activation J. Immunol., April 15, 2009; 182(8): 4686 - 4695. [Abstract] [Full Text] [PDF] C. B. Mathias, E.-J. Freyschmidt, B. Caplan, T. Jones, D. Poddighe, W. Xing, K. L. Harrison, M. F. Gurish, and H. C. 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