DOCK2 Is Essential for Antigen-Induced Translocation of TCR and Lipid Rafts, but Not PKC-[theta] and LFA-1, in T Cells

DOCK2 is a mammalian homolog ofCaenorhabditis elegansCED-5 andDrosophila melanogasterMyoblast City which are known to regulate actin cytoskeleton. DOCK2 is critical for lymphocyte migration, yet the role of DOCK2 in TCR signaling remains unclear. We show here that DOCK2 is essential for TCR-mediated...

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Veröffentlicht in:Immunity (Cambridge, Mass.) Mass.), 2003-07, Vol.19 (1), p.119
Hauptverfasser: Sanui, Terukazu, Inayoshi, Ayumi, Noda, Mayuko, Iwata, Eiko, Oike, Masahiro, Sasazuki, Takehiko, Fukui, Yoshinori
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container_issue 1
container_start_page 119
container_title Immunity (Cambridge, Mass.)
container_volume 19
creator Sanui, Terukazu
Inayoshi, Ayumi
Noda, Mayuko
Iwata, Eiko
Oike, Masahiro
Sasazuki, Takehiko
Fukui, Yoshinori
description DOCK2 is a mammalian homolog ofCaenorhabditis elegansCED-5 andDrosophila melanogasterMyoblast City which are known to regulate actin cytoskeleton. DOCK2 is critical for lymphocyte migration, yet the role of DOCK2 in TCR signaling remains unclear. We show here that DOCK2 is essential for TCR-mediated Rac activation and immunological synapse formation. In DOCK2-deficient T cells, antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, to the APC interface was severely impaired, resulting in a significant reduction of antigen-specific T cell proliferation. In addition, we found that the efficacy of both positive and negative selection was reduced in DOCK2-deficient mice. These results suggest that DOCK2 regulates T cell responsiveness through remodeling of actin cytoskeleton via Rac activation.
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subjects Apoptosis
Cell growth
Chemokines
Cytoskeleton
Kinases
Lipids
Lymphocytes
Microscopy
Peptides
Phosphorylation
Proteins
Rodents
T cell receptors
title DOCK2 Is Essential for Antigen-Induced Translocation of TCR and Lipid Rafts, but Not PKC-[theta] and LFA-1, in T Cells
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