Abstract
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.
Original language | English |
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Pages (from-to) | 157-166 |
Number of pages | 10 |
Journal | Immunity |
Volume | 17 |
Issue number | 2 |
DOIs | |
Publication status | Published - Aug 2002 |
ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases
- Immunology