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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.
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IMMUNOBIOLOGY
IgE- and IgE+Ag-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
From the Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA; the Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, CT; the Max Planck Institute for Experimental Endocrinology, Hannover, Germany; and the Department of Laboratory Medicine, University of California, San Francisco.
Mast cells are the major effector cells for immediate hypersensitivity and chronic allergic reactions. These cells accumulate in mucosal tissues of allergic reactions, where immunoglobulin E (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 efficiently activate mast cells can promote the migration of mast cells in the absence of antigen. IgE- and IgE+Ag-mediated migration involves an autocrine/paracrine secretion of soluble factors including adenosine, leukotriene B4, and several chemokines. Their secretion depends on 2 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. (Blood. 2005;105:3222-3229)
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