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Blood, 15 December 2005, Vol. 106, No. 13, pp. 4241-4248. Prepublished online as a Blood First Edition Paper on August 25, 2005; DOI 10.1182/blood-2005-04-1358. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-04-1358v1 106/13/4241    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 Nishimoto, H. Articles by Kawakami, T. Search for Related Content PubMed PubMed Citation Articles by Nishimoto, H. Articles by Kawakami, T. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Costimulation of mast cells by 4-1BB, a member of the tumor necrosis factor receptor superfamily, with the high-affinity IgE receptor Hajime Nishimoto, Seung-Woo Lee, Hong Hong, Karen G. Potter, Mari Maeda-Yamamoto, Tatsuya Kinoshita, Yuko Kawakami, Robert S. Mittler, Byoung S. Kwon, Carl F. Ware, Michael Croft, and Toshiaki Kawakami From the Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA; the Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA; the National Institute of Vegetable and Tea Science, National Agriculture Research Organization, Shizuoka, Japan; the Emory Vaccine Research Center, Emory University School of Medicine, Atlanta, GA; and the Immunomodulation Research Center, University of Ulsan, Ulsan, Korea. Mast cells are the major effector-cell type for immediate hypersensitivity and other forms of allergic reactions. Expression of 4-1BB, a member of the tumor necrosis factor receptor superfamily, is induced at mRNA and protein levels on stimulation through the high-affinity receptor for immunoglobulin E (IgE; FcRI). In this study, we present evidence that agonistic anti-4-1BB antibodies can enhance FcRI-induced cytokine production and secretion. Consistent with this, 4-1BB-deficient mast cells exhibit reduced degranulation and cytokine production on FcRI stimulation. Analysis of 4-1BB ligand (4-1BBL)-deficient cells supported this notion. As a potential mechanism for these defects, we identified a defect in Ca2+ flux induced by FcRI stimulation. The defective Ca2+ flux could be accounted for by the reduced activity of Lyn/Btk/phospholipase C-2 pathway and constitutive interactions between 4-1BB and Lyn. Therefore, FcRI-inducible 4-1BB plays a costimulatory function together with FcRI stimulation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Q.-T. Nguyen, S.-A Ju, S.-M. Park, S.-C. Lee, H. Yagita, I. H. Lee, and B.-S. Kim Blockade of CD137 Signaling Counteracts Polymicrobial Sepsis Induced by Cecal Ligation and Puncture Infect. Immun., September 1, 2009; 77(9): 3932 - 3938. [Abstract] [Full Text] [PDF] S. A. Boehme, K. Franz-Bacon, E. P. Chen, T. W. Ly, Y. Kawakami, and K. B. Bacon Murine bone marrow-derived mast cells express chemoattractant receptor-homologous molecule expressed on T-helper class 2 cells (CRTh2) Int. Immunol., June 1, 2009; 21(6): 621 - 632. [Abstract] [Full Text] [PDF] S.-C. Lee, S.-A Ju, B.-H. Sung, S.-K. Heo, H. R. Cho, E. A. Lee, J. D. Kim, I. H. Lee, S.-M. Park, Q. T. Nguyen, et al. 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