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

Int Immunol. 2003 Dec;15(12):1431-40. doi: 10.1093/intimm/dxg148.

Abstract

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 (FcepsilonRI) 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 FcepsilonRI-triggered total protein tyrosine phosphorylation, and protein tyrosine phosphorylation of FcepsilonRIbeta and Syk were not affected by WASP deficiency. However, tyrosine phosphorylation of phospholipase Cgamma and Ca(2+) 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 FcepsilonRI-mediated granule exocytosis, cytokine production and cytoskeletal changes in mast cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Actins / analysis
  • Actins / metabolism
  • Animals
  • Blotting, Western
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / metabolism
  • Calcium / metabolism
  • Cell Degranulation / physiology
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics
  • Cell Surface Extensions / drug effects
  • Dinitrophenols / immunology
  • Dinitrophenols / pharmacology
  • Female
  • Flow Cytometry
  • Histamine / blood
  • Immunization, Passive
  • Immunoglobulin E / analysis
  • Immunoglobulin E / immunology
  • Immunoglobulin E / pharmacology
  • Interleukin-3 / pharmacology
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • JNK Mitogen-Activated Protein Kinases
  • Male
  • Mast Cells / chemistry
  • Mast Cells / physiology*
  • Mice
  • Mice, Knockout
  • Microscopy, Fluorescence
  • Mitogen-Activated Protein Kinases / metabolism
  • Nerve Tissue Proteins / analysis
  • Phospholipase C gamma
  • Phosphorylation
  • Protein Serine-Threonine Kinases / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Proteins / analysis
  • Proteins / genetics
  • Proteins / physiology*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Receptor Aggregation / immunology
  • Receptors, IgE / metabolism
  • Receptors, IgE / physiology*
  • Serum Albumin / pharmacology
  • Signal Transduction / physiology*
  • Tumor Necrosis Factor-alpha / metabolism
  • Type C Phospholipases / metabolism
  • Wiskott-Aldrich Syndrome Protein
  • Wiskott-Aldrich Syndrome Protein, Neuronal
  • beta-N-Acetylhexosaminidases / metabolism

Substances

  • Actins
  • Dinitrophenols
  • Interleukin-3
  • Interleukin-6
  • Nerve Tissue Proteins
  • Proteins
  • Proto-Oncogene Proteins
  • Receptors, IgE
  • Serum Albumin
  • Tumor Necrosis Factor-alpha
  • Was protein, mouse
  • Wasl protein, mouse
  • Wiskott-Aldrich Syndrome Protein
  • Wiskott-Aldrich Syndrome Protein, Neuronal
  • dinitrophenyl-human serum albumin conjugate
  • Immunoglobulin E
  • Histamine
  • Protein-Tyrosine Kinases
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • Type C Phospholipases
  • Phospholipase C gamma
  • beta-N-Acetylhexosaminidases
  • Calcium