Wiskott-Aldrich syndrome protein regulates lipid raft dynamics during immunological synapse formation

Immunity. 2002 Aug;17(2):157-66. doi: 10.1016/s1074-7613(02)00360-6.


Immunological synapse assembly relies on the clustering of lipid rafts and is required for optimal T cell activation. We demonstrate that the Wiskott-Aldrich syndrome protein (WASP) is recruited to lipid rafts immediately after TCR and CD28 triggering and is required for the movements of lipid rafts. T cells from Wiskott-Aldrich syndrome (WAS) patients, lacking WASP, proliferate poorly after TCR/CD28 activation and have impaired capacities to cluster the lipid raft marker GM1 and to upregulate GM1 cell surface expression. T cell proliferation and lipid raft clustering are restored by retroviral transfer of the WASP gene. These results demonstrate that WASP plays a central role in the movements of lipid rafts and identify a potential mechanism underlying the T cell defect affecting WAS patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD28 Antigens / immunology
  • Calcium
  • Cell Division
  • Cells, Cultured
  • G(M1) Ganglioside / immunology
  • Humans
  • Lymphocyte Activation / immunology
  • Membrane Microdomains / immunology*
  • Proteins / genetics
  • Proteins / immunology*
  • Receptors, Antigen, T-Cell / immunology
  • Wiskott-Aldrich Syndrome / genetics
  • Wiskott-Aldrich Syndrome / immunology*
  • Wiskott-Aldrich Syndrome Protein


  • CD28 Antigens
  • Proteins
  • Receptors, Antigen, T-Cell
  • WAS protein, human
  • Wiskott-Aldrich Syndrome Protein
  • G(M1) Ganglioside
  • Calcium