The Wiskott-Aldrich Syndrome Protein Acts Downstream of CD2 and the CD2AP and PSTPIP1 Adaptors to Promote Formation of the Immunological Synapse

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• 作者：Karen Badour ; Jinyi Zhang ; Fabio Shi ; Mary K. H. McGavin ; Vik Rampersad ; Lynne A. Hardy ; Deborah Field and Katherine A. Siminovitch
• 刊名：Immunity
• 出版年：2003
• 出版时间：January 2003
• 年：2003
• 卷：18
• 期：1
• 页码：141-154
• 全文大小：1032 K

文摘

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.