Dynamin 2 regulates T cell activation by controlling actin polymerization at the immunological synapse

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作者
Timothy S Gomez
Michael J Hamann
Sean McCarney
Doris N Savoy
Casey M Lubking
Michael P Heldebrant
Christine M Labno
David J McKean
Mark A McNiven
Janis K Burkhardt
Daniel D Billadeau
机构
[1] Mayo Clinic College of Medicine,Department of Immunology
[2] Division of Oncology Research Mayo Clinic College of Medicine,Department of Pathology
[3] Children's Hospital of Philadelphia and the University of Pennsylvania,Department of Pathology
[4] University of Chicago,Department of Biochemistry and Molecular Biology
[5] Mayo Clinic College of Medicine,undefined
来源
Nature Immunology | 2005年 / 6卷
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摘要
Actin reorganization at the immunological synapse is required for the amplification and generation of a functional immune response. Using small interfering RNA, we show here that dynamin 2 (Dyn2), a large GTPase involved in receptor-mediated internalization, did not alter antibody-mediated T cell receptor internalization but considerably affected T cell receptor–stimulated T cell activation by regulating multiple biochemical signaling pathways and the accumulation of F-actin at the immunological synapse. Moreover, Dyn2 interacted directly with the Rho family guanine nucleotide exchange factor Vav1, and this interaction was required for T cell activation. These data identify a functionally important interaction between Dyn2 and Vav1 that regulates actin reorganization and multiple signaling pathways in T lymphocytes.
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页码:261 / 270
页数:9
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