| Autor: |
Badour K; Department of Medical Genetics and Microbiology, University of Toronto, 600 University Avenue, Toronto, M5G 1X5 Ontario, Canada., Zhang J, Shi F, McGavin MK, Rampersad V, Hardy LA, Field D, Siminovitch KA |
| Jazyk: |
angličtina |
| Zdroj: |
Immunity [Immunity] 2003 Jan; Vol. 18 (1), pp. 141-54. |
| DOI: |
10.1016/s1074-7613(02)00516-2 |
| Abstrakt: |
The Wiskott-Aldrich syndrome protein (WASp) couples actin cytoskeletal rearrangement to T cell activation, but the mechanisms involved are unknown. Here, we show that antigen-induced formation of T cell:APC conjugates and synapses is abrogated in WASp-deficient T cells and that CD2 engagement evokes interactions between the proline-rich region required for WASp translocation to the synapse and the PSTPIP1 adaptor SH3 domain and between the PSTPIp1 coiled-coil domain and both CD2 and another CD2-binding adaptor, CD2AP. The induced colocalization of these proteins at the synapse is disrupted by expression of coiled-coil domain-deleted PSTPIP1. These data, together with the impairment in CD2-induced actin polymerization observed in WASp-deficient cells, suggest that PSTPIP1 acts downstream of CD2/CD2AP to link CD2 engagement to the WASp-evoked actin polymerization required for synapse formation and T cell activation. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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