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Labno, Christine M.; Lewis, Carol M.; You, Daoqi; Leung, Daisy W.; Takesono, Ana; Kamberos, Natalie; Seth, Abhinav; Finkelstein, Lisa D.; Rosen, Michael K.; Schwartzberg, Pamela L.; Burkhardt, Janis K.
CB/Current biology, 09/2003, Letnik: 13, Številka: 18Journal Article
Actin polymerization at the immune synapse is required for T cell activation and effector function; however, the relevant regulatory pathways remain poorly understood. We showed previously that binding to antigen presenting cells (APCs) induces localized activation of Cdc42 and Wiskott-Aldrich Syndrome protein (WASP) at the immune synapse 1. Several lines of evidence suggest that Tec kinases could interact with WASP-dependent actin regulatory processes 2. Since T cells from Rlk−/−, Itk−/−, and Rlk−/− × Itk−/− mice have defects in signaling and development 3, we asked whether Itk or Rlk function in actin polymerization at the immune synapse. We find that Itk−/− and Rlk−/− × Itk−/− T cells are defective in actin polymerization and conjugate formation in response to antigen-pulsed APCs. Itk functions downstream of the TCR, since similar defects were observed upon TCR engagement alone. Using conformation-specific probes, we show that although the recruitment of WASP and Arp2/3 complex to the immune synapse proceeds normally, the localized activation of Cdc42 and WASP is defective. Finally, we find that the defect in Cdc42 activation likely stems from a requirement for Itk in the recruitment of Vav to the immune synapse. Our results identify Itk as a key element of the pathway leading to localized actin polymerization at the immune synapse.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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