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Blood, 15 April 2005, Vol. 105, No. 8, pp. 3222-3229. Prepublished online as a Blood First Edition Paper on January 6, 2005; DOI 10.1182/blood-2004-11-4205. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2004-11-4205v1 105/8/3222    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 Kitaura, J. Articles by Kawakami, T. Search for Related Content PubMed PubMed Citation Articles by Kitaura, J. Articles by Kawakami, T. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 12, 2004 Accepted December 19, 2004 IgE- and IgE/antigen-mediated mast cell migration in an autocrine/paracrine fashion Jiro Kitaura, Tatsuya Kinoshita, Masaaki Matsumoto, Shaun Chung, Yuko Kawakami, Michael Leitges, Dianqing Wu, Clifford A Lowell, and Toshiaki Kawakami* Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, California, USA Max Planck Institute for Experimental Endocrinology, Hannover, Germany Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut, USA Department of Laboratory Medicine, University of California, San Francisco, California, USA * Corresponding author; email: toshi{at}.liai.org. Mast cells are the major effector cells for immediate hypersensitivity and chronic allergic reactions. These cells accumulate in mucosal tissues of allergic reactions, where IgE is produced locally. Here we provide evidence that, in addition to antigen that can attract IgE-bound mast cells, the type of IgE molecules that can efficiently activate mast cells can promote the migration of mast cells in the absence of antigen. IgE- and IgE/antigen-mediated migration involves an autocrine/paracrine secretion of soluble factors including adenosine, leukotriene B4, and several chemokines. Their secretion depends on two tyrosine kinases, Lyn and Syk, and they are agonists of G-protein coupled receptors and signal through phosphatidylinositol 3-kinase , leading to mast cell migration. In mouse experiments, naive mast cells are attracted to IgE and IgE-sensitized mast cells are attracted to antigen. Therefore, IgE and antigen are implicated in mast cell accumulation at allergic tissue sites with local high IgE levels. 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Kitaura Mast Cell Survival and Activation by IgE in the Absence of Antigen: A Consideration of the Biologic Mechanisms and Relevance J. Immunol., October 1, 2005; 175(7): 4167 - 4173. [Abstract] [Full Text] [PDF] C. L. Weller, S. J. Collington, J. K. Brown, H. R.P. Miller, A. Al-Kashi, P. Clark, P. J. Jose, A. Hartnell, and T. J. Williams Leukotriene B4, an activation product of mast cells, is a chemoattractant for their progenitors J. Exp. Med., June 20, 2005; 201(12): 1961 - 1971. [Abstract] [Full Text] [PDF]

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