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International Immunology, Vol. 15, No. 12, pp. 1431-1440, December 2003
© 2003 Japanese Society for Immunology

FEATURED ARTICLE OF THE MONTH

Impaired signaling via the high-affinity IgE receptor in Wiskott–Aldrich syndrome protein-deficient mast cells

Vadim I. Pivniouk1,5, Scott B. Snapper2, Alexander Kettner1, Harri Alenius1, Dhafer Laouini1, Hervé Falet3, John Hartwig3, Frederick W. Alt4 and Raif S. Geha1

1 Division of Immunology, Children’s Hospital, 2 Division of Gastroenterology, Massachusetts General Hospital, 3 Division of Hematology, Brigham and Women’s Hospital, and 4 Howard Hughes Medical Institute, Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA 5 Present address: Department of Cell Biology and Anatomy, University of Arizona, Tucson, AZ 85724-5030, USA

Correspondence to: R. S. Geha; E-mail: raif.geha{at}tch.harvard.edu
Transmitting editor: S. J. Galli

Wiskott–Aldrich syndrome protein (WASP) is the product of the gene deficient in boys with X-linked Wiskott–Aldrich syndrome. We assessed the role of WASP in signaling through the high-affinity IgE receptor (Fc{epsilon}RI) using WASP-deficient mice. IgE-dependent degranulation and cytokine secretion were markedly diminished in bone marrow-derived mast cells from WASP-deficient mice. Upstream signaling events that include Fc{epsilon}RI-triggered total protein tyrosine phosphorylation, and protein tyrosine phosphorylation of Fc{epsilon}RIß and Syk were not affected by WASP deficiency. However, tyrosine phosphorylation of phospholipase C{gamma} and Ca2+ mobilization were diminished. IgE-dependent activation of c-Jun N-terminal kinase, cell spreading and redistribution of cellular F-actin in mast cells were reduced in the absence of WASP. We conclude that WASP regulates Fc{epsilon}RI-mediated granule exocytosis, cytokine production and cytoskeletal changes in mast cells.

Keywords: allergy and immunology, cell degranulation, receptor-mediated signal transduction, Wiskott–Aldrich syndrome


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